Loading...

Table of Content

    08 May 2026, Volume 30 Issue 13 Previous Issue    Next Issue
    For Selected: Toggle Thumbnails
    Effect of zoledronic acid on jaw bone marrow mesenchymal stem cells in mice with bisphosphonate-related osteonecrosis of the jaw
    Li Pengli, Yang Yanmei, Hu Yawen, Liu Hongqi, Wang Manyi, Yan Jianfei, Gu Bin
    2026, 30 (13):  3217-3225.  doi: 10.12307/2026.308
    Abstract ( 51 )   PDF (2315KB) ( 17 )   Save
    BACKGROUND: Bisphosphonates, as the core drugs of anti-bone resorption therapy, are widely used in the treatment of metabolic bone diseases. However, long-term use can cause the complications of bisphosphonate related osteonecrosis of the jaw. The traditional pathogenesis focuses on the inhibitory effect of bisphosphonates on osteoclasts, but it is difficult to fully explain the pathological development of osteonecrosis. Compared with the relatively mature osteoclast research, there are fewer reports on the effects of bisphosphonates on the biological characteristics and functions of osteoblast-related cells, and there are differences between some reports. This difference may be due to the experimental system, drug concentration and cell source, highlighting the necessity of conducting systematic and standardized research.
    OBJECTIVE: To investigate the effect of the third-generation bisphosphonate-zoledronic acid commonly used in clinical practice on the healing of tooth extraction sockets and the proliferation, migration and osteogenic differentiation of bone marrow mesenchymal stem cells derived from the jaw in mice.
    METHODS: Sixteen C57B/6J male mice were randomly divided into control group and experimental group. The experimental group was intraperitoneally injected with zoledronic acid combined with subcutaneous injection of dexamethasone; the control group was injected with the same amount of PBS. The left maxillary first molars of all mice were extracted after 2 weeks of injection, and the samples were sacrificed after 2 weeks of injection. The bone reconstruction and mucosal healing of the tooth extraction socket were observed by general observation of the wound of the tooth extraction socket, Micro CT imaging and three-dimensional reconstruction analysis, and hematoxylin-eosin staining. Bone marrow mesenchymal stem cells derived from the mandibular bones of the two groups of mice were isolated and cultured. After normal culture and osteogenic induction culture, the effects of zoledronic acid on cell proliferation, migration and osteogenic differentiation were observed by CCK-8 assay, qPCR, western blot assay, alkaline phosphatase staining, and Alizarin red staining.
    RESULTS AND CONCLUSION: (1) Compared with the control group, the bone and mucosa of the tooth extraction socket in the experimental group were poorly healed, and the inflammatory cell infiltration was more obvious. (2) Compared with the control group, the proliferation and migration abilities of bone marrow mesenchymal stem cells derived from the jaw in the experimental group were significantly inhibited (P < 0.05). (3) Compared with the control group, the alkaline phosphatase staining of bone marrow mesenchymal stem cells derived from the jaw in the experimental group was weaker, the number of calcium nodules decreased, and the expressions of alkaline phosphatase, bone sialic protein 2, type I collagen α1 chain and Runt-related transcription factor 2 were decreased (P < 0.05). The results showed that zoledronic acid could adversely affect the healing of the tooth extraction socket in mice, which may be related to the inhibition of the proliferation, migration and osteogenic differentiation of bone marrow mesenchymal stem cells derived from the jaw.
    Figures and Tables | References | Related Articles | Metrics
    Extracellular matrix stiffness affects the proliferation activity of bone marrow stromal stem cells
    Gao Feng, Wang Jiliang, Wang Hongbo, Yang Yongsheng, Liu Yuan, Fu Su
    2026, 30 (13):  3226-3232.  doi: 10.12307/2026.583
    Abstract ( 50 )   PDF (2351KB) ( 13 )   Save
    BACKGROUND: In tissue engineering bone construction, the physical properties of the scaffold can directly affect the activity and repair effect of seed cells, among which extracellular matrix hardness is a key factor affecting seed cell proliferation activity. Primary cilia and YAP proteins have been shown to be classical mechanoreceptors and downstream transduction factors, which may directly mediate this mechanism.
    OBJECTIVE: To investigate the regulatory effect of extracellular matrix hardness on the proliferation activity of bone marrow stromal stem cells and the related mechanisms.
    METHODS: Bone marrow stromal stem cells were passaged and seeded under different hardness of polydimethylsiloxane extracellular matrix conditions (soft, median, and rigid) for culture. Cell proliferation activity was detected using CCK-8 assay. Transcriptional activity of proliferation genes myc and CCND1 was measured using qRT-PCR. Activation of Wnt/β-catenin pathway was evaluated using western blot assay. Primary cilia and YAP protein expression levels were evaluated by acetylated α-tubulin and YAP immunofluorescence staining. After passage, bone marrow stromal stem cells were inoculated on polydimethylsiloxane-based membranes of different hardness (soft and hard) for culture. Then siRNA was used to interfere with YAP protein expression. Western blot assay was used to detect YAP, phosphorylated GSK-3β, and β-catenin protein expression. qRT-PCR was used to detect the transcriptional activity of c-myc and CCND1. The length of primary cilia was analyzed after immunofluorescence staining of acetylated α-tubulin.
    RESULTS AND CONCLUSION: The cell proliferation activity, c-myc and CCND1 transcriptional activities under hard polydimethylsiloxane were significantly higher than those under soft and medium hard polydimethylsiloxane, and the activation of Wnt/β-catenin pathway was stronger than that under soft and medium hard polydimethylsiloxane. Immunofluorescence staining results showed that hard polydimethylsiloxane induced the shortening of primary cilia and the increase of YAP protein-positive cells. After interfering with YAP protein expression by siRNA, the inter-group differences in YAP, phosphorylated GSK-3β, β-catenin protein expression, and c-myc and CCND1 transcriptional activities disappeared, accompanied by the disappearance of primary cilia length differences. The results show that the hardness of the extracellular matrix directly regulates the proliferation activity of bone marrow stromal stem cells through the new mechanism of YAP protein/primary cilia.

    Figures and Tables | References | Related Articles | Metrics
    Isolation, cultivation, identification, and induction of M1/M2 polarization in bone marrow-derived macrophages from C57BL/6 mice
    Tan Yuhang, Li Bo, Tang Minghong, Sun Zeyu, Luo Xu
    2026, 30 (13):  3233-3241.  doi: 10.12307/2026.087
    Abstract ( 168 )   PDF (4628KB) ( 46 )   Save
    BACKGROUND: Macrophage polarization demonstrates significant potential in disease treatment, particularly in areas such as cancer, inflammation, and autoimmune diseases. Establishing standardized in vitro models can lay the groundwork for in-depth research into the mechanisms of macrophage polarization.
    OBJECTIVE: To observe the in vitro growth characteristics of bone marrow-derived macrophages from C57BL/6 mice and to establish a standardized in vitro model for M1 and M2 macrophage polarization.
    METHODS: Femurs and tibias of C57BL/6 mice were aseptically separated, and the contents of the bone marrow cavity were collected. After filtering through a mesh and lysing erythrocytes, the contents were resuspended in high-glucose DMEM containing 20 ng/mL macrophage colony-stimulating factor and inoculated in 6-well plates according to experimental requirements. On day 7, they were differentiated into mature mouse bone marrow-derived macrophages (M0 type). Then, 100 ng/mL lipopolysaccharide was used to induce polarization of M1 macrophages, and 20 ng/mL interleukin-4 was used to induce polarization of M2 macrophages. Flow cytometry and RT-qPCR were used to detect the expression of corresponding markers of macrophages in different polarization states. Western blot assay was used to detect the expression of M1 macrophage marker pathway proteins p-STAT1 and STAT1 and M2 macrophage marker pathway proteins p-STAT6 and STAT6.
    RESULTS AND CONCLUSION: (1) After stimulation with 20 ng/mL macrophage colony-stimulating factor for 7 days, the positive staining rate of macrophage surface marker F4/80 by flow cytometry reached 98.1%. (2) After bone marrow-derived macrophages were stimulated with 100 ng/mL lipopolysaccharide for 6 hours, the positive staining rates of F4/80 and CD86 were approximately 35%, and the mRNA expressions of M1 macrophage markers inducible nitric oxide synthase, interleukin-6, macrophage inflammatory protein-1α, and monocyte chemoattractant protein-1 by RT-qPCR were significantly higher than those in the control group (P < 0.01). (3) After bone marrow-derived macrophages were stimulated with 20 ng/mL interleukin-4 for 24 hours, the mean fluorescence intensity of CD206 was significantly increased, and the mRNA expressions of M2 macrophage markers Chi3l3 (Ym1), interleukin-10, and arginase-1 by RT-qPCR were significantly higher than those in the control group (P < 0.01). (4) Western blot assay results showed that lipopolysaccharide-induced M1 macrophages' signature pathway p-STAT1 was significantly activated; interleukin-4-induced M2 macrophages' landmark pathway p-STAT6 was significantly activated. The above results indicate that lipopolysaccharide and interleukin-4 effectively induce bone marrow-derived macrophages to polarize into M1 and M2 macrophages, respectively.
    Figures and Tables | References | Related Articles | Metrics
    Chemokine receptor 7-bone marrow mesenchymal stem cells combined with porcine small intestinal submucosa promote skin repair in rats
    Fan Meirong, Li Guangqi, Song Xumei, Yan Xin, Sui Ruizhi
    2026, 30 (13):  3242-3249.  doi: 10.12307/2026.058
    Abstract ( 61 )   PDF (2171KB) ( 13 )   Save
    BACKGROUND: The clinical outcomes of autologous and allogeneic skin transplants, which are commonly used for repairing skin lesions, are often suboptimal. In recent years, advancements in tissue engineering have provided new hope for skin repair. Nevertheless, the regeneration of blood vessels within skin tissue engineering remains a significant challenge. Porcine small intestinal submucosa and bone marrow-derived mesenchymal stem cells are widely utilized natural extracellular matrix biomaterials and seed cells in current tissue engineering research. Chemokine receptor 7 is a cytokine that can promote angiogenesis.
    OBJECTIVE: To observe the repair effect and angiogenesis ability of chemokine receptor 7-bone marrow mesenchymal stem cells-porcine small intestinal submucosa membrane on rat back skin damage.
    METHODS: (1) The adenovirus vector overexpressing chemokine receptor 7 was used to transfect bone marrow mesenchymal stem cells. The transfection efficiency was evaluated using western blot assay and RT-qPCR. (2) The bone marrow mesenchymal stem cells overexpressing chemokine receptor 7 were co-cultured with porcine small intestinal submucosa. Cytocompatibility was assessed through scanning electron microscopy and live/dead cell staining. (3) 12 SD rats were utilized to establish a skin defect animal experimental model, and chemokine receptor 7-bone marrow mesenchymal stem cells-porcine small intestinal submucosa (experimental group) and porcine small intestinal submucosa (control group) were placed in the rat skin defect, and the wound healing was observed 1, 3, 7, and 14 days after modeling. The expression of vascular endothelial growth factor protein in the wound healing tissue was detected by western blot assay at 7 and 14 days after modeling, and the expression of CD31 and proliferating cell nuclear antigen protein in the wound tissue was detected by immunohistochemical staining.
    RESULTS AND CONCLUSION: (1) Bone marrow mesenchymal stem cells overexpressing chemokine receptor 7 were successfully constructed by adenovirus-mediated transfection. The protein and mRNA expressions of chemokine receptor 7 in the chemokine receptor 7 transfected group were significantly upregulated compared with those in the control group and the empty vector group (P < 0.001). (2) Scanning electron microscopy observation and live-dead cell staining results showed that bone marrow mesenchymal stem cells overexpressing chemokine receptor 7 grew well on the surface of the submucosal membrane of the porcine small intestine, and the two had good compatibility. (3) Compared with the control group, the wound area of the experimental group was significantly reduced (P < 0.05). The protein expression levels of vascular endothelial growth factor, CD31, and proliferating cell nuclear antigen in the wound healing tissue of the experimental group were higher than those in the control group (P < 0.05), indicating that the ability of chemokine receptor 7-bone marrow mesenchymal stem cells-porcine small intestinal submucosal membrane to promote wound angiogenesis was strong. 
    Figures and Tables | References | Related Articles | Metrics
    Function of human amniotic mesenchymal stem cell exosomes in repairing submandibular gland epithelial cells after radiation injury in SD rats
    Zhang Ligang, Liu Tao, Yi Jie, Zhang Nini, Yao Li, Huang Guilin, Hu Xiaohua, Dai Min
    2026, 30 (13):  3250-3257.  doi: 10.12307/2026.088
    Abstract ( 50 )   PDF (2086KB) ( 8 )   Save
    BACKGROUND: Hypoxia preconditioning can increase extracellular vesicles, growth factors, anti-inflammatory and immunosuppressive factors in the parasecretory secretions of mesenchymal stem cells. Exosomes derived from human amniotic mesenchymal stem cells preconditioned with hypoxia are expected to play a better therapeutic role in tissue damage repair.
    OBJECTIVE: To observe the repair effect of exosomes from human amniotic mesenchymal stem cells preconditioned with hypoxia on radiation-induced submandibular gland epithelial cell damage. 
    METHODS: The passage 3 human amniotic mesenchymal stem cells were divided into two groups: hypoxia and normoxia. They were pretreated with hypoxia (1% O2 by volume) and normoxia (20% O2 by volume) for 48 hours, respectively. Then, normoxic and hypoxic human amniotic mesenchymal stem cell exosomes were extracted from the culture supernatant of human amniotic mesenchymal stem cells by modified ultrahigh-speed centrifugation. The submandibular gland epithelial cells of SD newborn rats were divided into blank control group, radiation control group, normoxic drug group, and hypoxic drug group. The submandibular gland epithelial cells were irradiated with 5 Gy to establish the radiation-damaged submandibular gland epithelial cell model. On this basis, normoxic and hypoxic human amniotic mesenchymal stem cell exosomes were added to the normoxic drug group and the hypoxic drug group and co-cultured with the submandibular gland epithelial cells for 3 days. The proliferation activity of the submandibular gland epithelial cells of the rats in each group was detected by CCK-8 assay. The alpha amylase content in the supernatant of the submandibular gland epithelial cells of the rats in each group was determined by ELISA. RT-qPCR was used to detect the expression of aquaporin 5 mRNA in the submandibular gland epithelial cells of the rats in each group.
    RESULTS AND CONCLUSION: (1) The cell proliferation activity of the radiation control group was significantly decreased compared to the blank control group (P < 0.05). The cell proliferation activity of the normoxic and hypoxic drug groups significantly increased on days 2 and 3 compared to the radiation control group (P < 0.05). The cell proliferation activity of the hypoxic drug group was higher than that of the hypoxic drug group on the first day, and showed an increasing trend on the second and third days, but there was no statistical difference compared with the normoxic drug group (P > 0.05). (2) The content of alpha amylase in the radiation control group was significantly reduced compared with the blank control group (P < 0.05). The levels of alpha amylase in the normoxic and hypoxic drug groups were significantly higher than those in the radiation control group (P < 0.05). Compared with the normoxic drug group, the hypoxic drug group showed an increasing trend in alpha amylase content, but there was no statistical difference (P > 0.05). (3) The mRNA expression of aquaporin 5 in the radiation control group was significantly reduced compared to the blank control group (P < 0.05). The mRNA expression of aquaporin 5 in the normoxic and hypoxic drug groups was significantly increased compared with the radiation control group (P < 0.05). The mRNA expression of aquaporin 5 in the hypoxic drug group was slightly higher than that in the normoxic drug group, but there was no statistical difference (P > 0.05). These results indicate that extracellular vesicles from human amniotic mesenchymal stem cells pre-treated with normoxic and hypoxic conditions have a repairing effect on submandibular gland epithelial cells damaged by radiation, but there is no significant advantage in hypoxic human amniotic mesenchymal stem cell exosomes. 
    Figures and Tables | References | Related Articles | Metrics
    Wenshen Tongluo Zhitong decoction regulates the bone fat differentiation balance of bone marrow mesenchymal stem cells through exosomal miR-342-3p
    Wumiti·Taxi, Wang Lining, Li Muzhe, Sun Jie, Chen Shuangliu, Zhu Yihua, Zhou Shijie, Ma Yong, Guo Yang
    2026, 30 (13):  3258-3269.  doi: 10.12307/2026.672
    Abstract ( 48 )   PDF (6480KB) ( 19 )   Save
    BACKGROUND: The potential role of traditional Chinese medicine and its active ingredients in regulating the function of exosomal miRNA has opened up a new way for the treatment of bone metabolic diseases. 
    OBJECTIVE: To investigate the effect and mechanism of Wenshen Tongluo Zhitong decoction in improving bone fat differentiation balance in bone marrow mesenchymal stem cells by regulating adipocyte derived exosome miR-342-3p. 
    METHODS: Adipose mesenchymal stem cells and bone marrow mesenchymal stem cells of 1-week-old SD rats were isolated and cultured. Adipose-derived mesenchymal stem cells were treated with serum containing Wenshen Tongluo Zhitong decoction, and then exosomes were extracted by high-speed centrifugation method. After exosomes were co-cultured with bone marrow mesenchymal stem cells for 48 hours, alkaline phosphatase staining, alizarin red staining, and oil red O staining were used to evaluate the bone-fat differentiation ability of bone marrow mesenchymal stem cells. High-throughput sequencing was used to screen differential miRNAs, and downstream target genes were analyzed by bioinformatics, and the expression of key miRNAs and target genes was verified by qPCR. qPCR was used to evaluate the effects of miR-342-3p and its target gene PDGFRα on the expression of osteogenic and adipogenic differentiation genes of bone marrow mesenchymal stem cells. Western blot assay was used to detect the effects of miR-342-3p and PDGFRα on the expression of downstream phosphoinositide 3-kinase/protein kinase B pathway proteins.
    RESULTS AND CONCLUSION: Wenshen Tongluo Zhitong decoction significantly promoted the secretion of exosomes derived from adipose mesenchymal stem cells and made them more easily taken up by bone marrow mesenchymal stem cells. Sequencing results showed that the expression of miR-342-3p in exosomes derived from adipose mesenchymal stem cells after Wenshen Tongluo Zhitong decoction intervention was the most obvious, which promoted the osteogenic differentiation of bone marrow mesenchymal stem cells (up-regulated Runx2 and Osterix mRNA expression) and inhibited adipogenic differentiation (down-regulated PPARγ and CEBPα mRNA expression) by targeting and inhibiting PDGFRα. miR-342-3p could promote the phosphorylation expression of phosphoinositide 3-kinase and protein kinase B, activate the phosphoinositide 3-kinase/protein kinase B signaling pathway, and regulate the balance of bone and fat differentiation of bone marrow mesenchymal stem cells. The above results indicate that Wenshen Tongluo Zhitong decoction regulates the balance of bone-fat differentiation of bone marrow mesenchymal stem cells by targeting the PDGFRα/phosphoinositide 3-kinase/protein kinase B axis through exosome miR-342-3p of adipose mesenchymal stem cells, which can provide a molecular mechanism basis for the prevention and treatment of osteoporosis with traditional Chinese medicine compound.
    Figures and Tables | References | Related Articles | Metrics
    Reduced graphene oxide improves endothelial differentiation efficiency and angiogenesis ability of adipose-derived stem cells
    Yao Jinfeng, Deng Mengzhao, Xie Tian, Chen Kan, Wang Haixia
    2026, 30 (13):  3270-3279.  doi: 10.12307/2026.134
    Abstract ( 44 )   PDF (2531KB) ( 47 )   Save
    BACKGROUND: Adipose-derived stem cells can differentiate into vascular endothelial cells in a specific induction environment and are ideal seed cells in the process of tissue engineering vascularization.
    OBJECTIVE: To explore the effect of reduced graphene oxide on the endothelial differentiation efficiency and angiogenesis ability of adipose-derived stem cells.
    METHODS: Firstly, reduced graphene oxide was prepared by green synthesis process and characterized by transmission electron microscopy, energy spectrum analysis and Fourier transform infrared spectroscopy. Different mass concentrations of reduced graphene oxide were co-cultured with adipose-derived stem cells, and the safe concentration range of reduced graphene oxide was determined by CCK8 assay. Then, the endothelial differentiation of adipose-derived stem cells was induced by reduced graphene oxide in a safe concentration range for different times. The expression of endothelial differentiation-related indicators of adipose-derived stem cells was detected by RT-qPCR and western blot assay. Finally, the tube formation and migration abilities of cells induced by reduced graphene oxide were evaluated by scratch test and tubule formation test.
    RESULTS AND CONCLUSION: (1) Reduced graphene oxide has a typical two-dimensional sheet structure, mainly containing carbon and oxygen elements, and characteristic absorption peaks related to oxygen-containing functional groups can be detected. (2) The results of CCK-8 assay showed that reduced graphene oxide at a concentration of 10 μg/mL or less had no effect on the cell viability of adipose-derived stem cells after 72 hours of culture. (3) The results of RT-qPCR and western blot assay show that reduced graphene oxide at a concentration of 10 μg/mL or less could significantly increase the expression of markers related to endothelial differentiation of adipose-derived stem cells after 6 and 9 days of induction, among which 5 μg/mL reduced graphene oxide induced 9 days, and the gene expression difference of endothelial differentiation markers was the greatest. (4) The results of scratch test and tubule formation test showed that compared with the blank group and the control group, the migration and tube formation abilities of cells in the reduced graphene oxide group were significantly enhanced. (5) The results show that green synthesized reduced graphene oxide can significantly improve the endothelial differentiation efficiency of adipose-derived stem cells, among which 5 μg/mL reduced graphene oxide induction for 9 days is the best time-concentration combination, and the induced differentiated cells have better angiogenesis function.
    Figures and Tables | References | Related Articles | Metrics
    Lipopolysaccharides regulate the function of human umbilical vein endothelial cells
    She Xu, Li Xiaojiang, Huang Haixia, Wan Lingling, Luo Qingqing
    2026, 30 (13):  3280-3287.  doi: 10.12307/2025.579
    Abstract ( 40 )   PDF (1707KB) ( 10 )   Save
    BACKGROUND: Vascular endothelial cell dysfunction is the core factor in the pathogenesis of preeclampsia. Lipopolysaccharide can be used to establish a rat model of preeclampsia, but the effect and mechanism on endothelial cells have not been fully clarified.
    OBJECTIVE: To investigate the effect of lipopolysaccharides on the function of human umbilical vein endothelial cells and its possible mechanism.
    METHODS: Human umbilical vein endothelial cells were divided into control group and lipopolysaccharides group. The functional changes of human umbilical vein endothelial cells after lipopolysaccharides treatment in both groups were detected by the following experiments: Cell adhesion test was used to detect the adhesion of monocytes to human umbilical vein endothelial cells. Tubule formation experiment was used to detect the tubule formation ability of human umbilical vein endothelial cells. The mRNA expression levels of nucleotide binding oligomerization domain-like receptor protein 3, interleukin-1β, 6-phosphofructo-2-kinase and endothelial nitric oxide synthase were detected by qPCR. Western blot assay was utilized to detect the protein expression levels of nucleotide binding oligomerization domain-like receptor protein 3, 6-phosphofructo-2-kinase 3, intercellular adhesion molecule 1, and endothelial nitric oxide synthase. Human umbilical vein endothelial cells were divided into control group, lipopolysaccharide group, and MCC950 (nucleotide binding oligomerization domain-like receptor protein 3 inhibitor) group. qPCR was used to detect the mRNA expression levels of nucleotide binding oligomerization domain-like receptor protein 3, interleukin-1β, 6-phosphofructo-2-kinase 3 and endothelial nitric oxide synthase.
    RESULTS AND CONCLUSION: (1) Compared with the control group, the expression of intercellular adhesion molecule-1 protein in lipopolysaccharides group increased (P < 0.05), and the adhesion of monocytes increased (P < 0.05), suggesting that human umbilical vein endothelial cells were activated and their adhesion ability was enhanced. (2) Compared with the control group, the tubule formation ability of human umbilical vein endothelial cells was inhibited in the lipopolysaccharides group (P < 0.05). (3) Compared with the control group, the mRNA and protein expression levels of endothelial nitric oxide synthase were decreased in the lipopolysaccharides group (P < 0.05); mRNA expression levels of nucleotide binding oligomerization domain-like receptor protein 3, interleukin-1β, and 6-phosphofructo-2-kinase, as well as the protein expression levels of nucleotide binding oligomerization domain-like receptor protein 3 and 6-phosphofructo-2-kinase 3 were increased (P < 0.05). (4) Compared with the lipopolysaccharides group, the mRNA expressions of interleukin-1β and 6-phosphofructo-2-kinase 3 were decreased, and the mRNA expression of endothelial nitric oxide synthase was increased in the MCC950 group (P < 0.05). The results suggest that lipopolysaccharides can cause dysfunction of human umbilical vein endothelial cells, which may be regulated by the nucleotide-binding oligomerization domain-like receptor protein 3/interleukin-1β/6-phosphofructo-2-kinase 3 pathway. 
    Figures and Tables | References | Related Articles | Metrics
    Regulation of antler stem cell exosomes miRNA-145 on inflammatory chondrocytes
    Jiang Yidi, Zhao Jianwei, Zhou Jue, Lyu Jinpeng, Wang Datao, Li Xunsheng, Yue Zhigang, Cui Bo, Sun Hongmei
    2026, 30 (13):  3288-3297.  doi: 10.12307/2026.322
    Abstract ( 55 )   PDF (3816KB) ( 10 )   Save
    BACKGROUND: In recent years, the research on the role of stem cell exosomes in the treatment of arthritis has attracted more and more attention. In the early stage, our research group found that the secretion of antler stem cells has the potential to repair cartilage injuries, but its specific function is still unclear. 
    OBJECTIVE: To explore the regulatory role and mechanisms of antler stem cell exosomes miRNA-145 in chondrocyte injury repair. 
    METHODS: A lentiviral vector system was employed to establish the antler stem cells overexpressing miRNA-145. Exosomes were extracted from these cells using ultracentrifugation. Rat chondrocytes were divided into five groups: blank control group, interleukin 1β group, exosomes + interleukin 1β group, empty vector transfected exosomes + interleukin 1β group, and miRNA-145 transfected exosomes + interleukin 1β group. Except for the blank control group, the chondrocytes in the other four groups were induced with interleukin 1β for 24 hours to establish an inflammatory cell model, and then treated with corresponding exosomes. CCK-8 assay was used to detect the cell proliferation level. The scratch test was used to detect the cell migration ability. qPCR and western blot assay were used to detect the expression levels of chondrocyte-related genes and proteins. 
    RESULTS AND CONCLUSION: (1) The exosomes exhibited a typical oval double-layer vesicle structure with diameters ranging from 50 to 150 nm, all of which expressed classical markers of exosomes, such as CD9, ALIX, and TSG101, and none of them expressed Calnexin. (2) Antler stem cell exosomes enhanced chondrocyte viability, cell mobility, type II collagen A1, transforming growth factor β1, SMAD3, SOX9 mRNA and protein expression levels, and reduced matrix metalloproteinase 13 mRNA expression level in the inflammatory environment. (3) miRNA-145 further decreased chondrocyte viability, cell mobility, type II collagen A1, transforming growth factor β1, SMAD3, SOX9 mRNA and protein expression, and further increased matrix metalloproteinase 13 mRNA expression in the inflammatory environment. (4) These results conclude that antler stem cell exosomes can promote chondrocyte repair through the transforming growth factor β1/SMAD3 signaling pathway, and overexpression of miRNA-145 inhibits chondrocyte repair. 
    Figures and Tables | References | Related Articles | Metrics
    Effect of miR-223-3p on biological behavior of tendon stem cells under hypoxic conditions
    Duan Cheng, Cheng Jie
    2026, 30 (13):  3298-3307.  doi: 10.12307/2026.728
    Abstract ( 40 )   PDF (4812KB) ( 6 )   Save
    BACKGROUND: The hypoxic microenvironment is a key regulator of tendon injury repair, but the molecular mechanism mediated by microRNAs (miRNAs) is not well understood.
    OBJECTIVE: To investigate the regulatory role and mechanism of miR-223-3p on the biological behavior of tendon stem cells under hypoxic conditions. 
    METHODS: (1) The rat third-generation tendon stem cells were divided into control group (O₂ concentration 21%) and hypoxia group (O₂ concentration 1%). After 48 hours of culture, CCK-8 assay was used to detect cell proliferation. Muse apoptosis detection kit was used to detect apoptosis rate. RT-qPCR and western blot assay were used to detect the protein and mRNA expressions of hypoxia-inducible factor-1α and vascular endothelial growth factor. (2) miR-223-3p targets were predicted by bioinformatics. The targeting and regulation relationship between miR-223-3p and VHL was verified by double luciferase assay. (3) The third-generation rat tendon stem cells were divided into five groups: normoxic miR-223-3p mimic group, normoxic mimic negative control group, normoxic inhibitor negative control group, hypoxic inhibitor negative control group, and hypoxic miR-223-3p inhibitor group. After culture under normoxia or hypoxia for 48 hours, the expression of hypoxia-inducible factor-1α, vascular endothelial growth factor, and VHL protein and mRNA was detected by RT-qPCR and western blot assay. Cell viability was determined by CCK-8 assay, and the apoptosis rate was analyzed by Muse cell apoptosis detection kit. The cell migration and invasion were evaluated by scratch assay and Transwell chamber assay.
    RESULTS AND CONCLUSION: (1) Compared with the control group, the tendon stem cell viability in the hypoxic group was significantly decreased (P < 0.001), and the apoptosis rate was significantly increased (P < 0.01). Compared with the control group, the mRNA expressions of miR-223-3p, hypoxia-inducible factor-1α and vascular endothelial growth factor in tendon stem cells in the hypoxic group were significantly increased (P < 0.01). The expressions of hypoxia-inducible factor-1α and vascular endothelial growth factor proteins in tendon stem cells in the hypoxia group were significantly increased (P < 0.01). (2) Bioinformatics predicted that VHL had potential binding sites with miR-223-3p. Dual-luciferase assay showed that miR-223-3p could bind to VHL targeting. (3) Functional experiments showed that knockdown of miR-223-3p could up-regulate the mRNA and protein expression of VHL in tendon stem cells, down-regulate the mRNA and protein expressions of hypoxia-inducible factor-1α and vascular endothelial growth factor (P < 0.01), improve the viability of tendon stem cells, reduce the rate of apoptosis, and promote cell migration and invasion (P < 0.01), while overexpression of miR-223-3p was the opposite and aggravated hypoxic damage, which may be related to the activation of hypoxia-inducible factor-1α/vascular endothelial growth factor/VHL signaling pathway. 
    Figures and Tables | References | Related Articles | Metrics
    Anti-inflammatory activity and mechanism of Lonicera japonica Thunb.-derived extracellular vesicle-like particles
    Chen Yuanjun, Lin Sixing, Ji Lichun, Li Dongxiao, Liao Guangzhi, Lin Xingdong
    2026, 30 (13):  3308-3320.  doi: 10.12307/2026.153
    Abstract ( 56 )   PDF (32465KB) ( 28 )   Save
    BACKGROUND: Recently, nanotechnology has shown potential in anti-inflammatory treatment, but nanodrug systems face challenges in production costs, process complexity, and biosafety. Chinese herbal medicine-derived vesicle technology, with advantages like abundant sources and good biocompatibility, has emerged as a new research hotspot in traditional Chinese medicine.
    OBJECTIVE: To explore the anti-inflammatory biological activity and mechanism of Lonicera japonica Thunb.-derived extracellular vesicle-like particles.
    METHODS: Lonicera japonica Thunb.-derived extracellular vesicle-like particles were extracted using ultracentrifugation and characterized. The uptake of Lonicera japonica Thunb.-derived extracellular vesicle-like particles by RAW264.7 cells and their biocompatibility were evaluated using CCK-8 assays, flow cytometry, and confocal microscopy. A lipopolysaccharide-induced RAW264.7 cell inflammation model was established to investigate the effects of Lonicera japonica Thunb.-derived extracellular vesicle-like particles on inflammatory mediators and macrophage phenotypes. Transcriptomics was used to elucidate the anti-inflammatory mechanisms of Lonicera japonica Thunb.-derived extracellular vesicle-like particles.
    RESULTS AND CONCLUSION: (1) Lonicera japonica Thunb.-derived extracellular vesicle-like particles had a particle size of (79.42±23.12) nm, with typical cup-shaped vesicle and membrane structures, and showed good stability in simulated gastrointestinal digestion. (2) Lonicera japonica Thunb.-derived extracellular vesicle-like particles were non-toxic to RAW264.7 cells, with an uptake rate exceeding 90% after 8 hours. (3) In inflammatory models, Lonicera japonica Thunb.-derived extracellular vesicle-like particles significantly reduced interleukin-6, interleukin-1β and cyclooxygenase-2 levels, inhibited M1 macrophage polarization, and restored interleukin-10 and CD206 levels. (4) Transcriptomic analysis suggests that Lonicera japonica Thunb.-derived extracellular vesicle-like particles exert anti-inflammatory effects by modulating key inflammatory signaling pathways such as tumor necrosis factor, nuclear factor κB, and Toll-like receptors. These findings demonstrate significant anti-inflammatory activity of Lonicera japonica Thunb.-derived extracellular vesicle-like particles, providing experimental evidence for their potential as a novel anti-inflammatory drug delivery system and offering a new option for treating inflammatory diseases.
    Figures and Tables | References | Related Articles | Metrics
    Impact and mechanism of proprotein convertase subtilisin/kexin type 9 on cholesterol efflux in human monocyte-derived foam cells
    Liao Fujun, Bao Hailong, Gong Caiwei, Liu Danan
    2026, 30 (13):  3321-3330.  doi: 10.12307/2026.623
    Abstract ( 37 )   PDF (4357KB) ( 17 )   Save
    BACKGROUND: Human proprotein convertase subtilisin/kexin type 9 (PCSK9), a key regulator of cholesterol metabolism, modulates cholesterol uptake and plasma lipid levels by binding to and promoting the degradation of the low-density lipoprotein receptor. Cholesterol efflux is mediated by transporters such as ATP-binding cassette transporter A1 (ABCA1) and scavenger receptor class B type I (SR-BI), with trafficking kinesin protein 2 (TRAK2) potentially acting as an adaptor protein in this process. Investigating whether PCSK9 regulates cholesterol efflux through the TRAK2/ABCA1 pathway provides novel insights into its role in atherosclerosis.
    OBJECTIVE: To explore the effect of PCSK9 on cholesterol efflux in human monocyte-derived macrophages and its underlying mechanisms.
    METHODS: THP-1 cells were centrifuged and added with phorbol ester for 48 hours to induce differentiation into THP-1-derived macrophages, and then incubated with serum-free medium containing oxidized low-density lipoprotein for 24 hours to induce foam cell formation. (1) The foam cells were divided into four groups: control group, PCSK9 protein group, negative control group (non-targeted siRNA transfected foam cells), and PCSK9 siRNA transfection group. RT-qPCR and western blot assay were used to detect the mRNA and protein expressions of TRAK2, ABCA1, ABCG1, and SR-BI. (2) The foam cells were divided into three groups: negative control group, TRAK2 siRNA transfection group, and (TRAK2+PCSK9) siRNA co-transfection group. RT-qPCR and western blot assay were used to detect the mRNA and protein expressions of ABCA1. (3) The foam cells were divided into eight groups: control group, PCSK9 protein group, PCSK9 siRNA transfection group, TRAK2 siRNA transfection group, ABCA1 siRNA transfection group, (TRAK2+PCSK9) siRNA co-transfection group, (PCSK9+ABCA1) siRNA co-transfection group, and (TRAK2+ABCA1) siRNA co-transfection group. 25-NBD-cholesterol was used to analyze the cholesterol efflux rate of foam cells. 
    RESULTS AND CONCLUSION: (1) The TRAK2 mRNA and protein expression levels in the PCSK9 group were higher than those in the control group (P < 0.05), whereas the expression levels of ABCA1, ABCG1, and SR-BI showed no significant difference compared to the control group. In the PCSK9 siRNA transfection group, TRAK2 mRNA and protein expression levels were lower than in the negative control group (P < 0.001 and P < 0.05, respectively), while ABCA1 mRNA and protein expression levels were higher than in the negative control group (P < 0.001); no significant difference was observed in the mRNA and protein expression levels of ABCG1 and SR-BI compared to the negative control group. (2) In the TRAK2 siRNA transfection group, ABCA1 mRNA and protein expression levels were higher than those in the negative control group (P < 0.001 and P < 0.05, respectively), and in the (TRAK2+PCSK9) siRNA group, ABCA1 mRNA and protein expression levels were higher than those in the negative control group (P < 0.001 and P < 0.05, respectively). There was no significant difference in ABCA1 mRNA and protein expression levels between the (TRAK2+PCSK9) siRNA group and the TRAK2 siRNA group. (3) There was no significant difference in cholesterol efflux between the PCSK9 group and the control group. Cholesterol efflux in the PCSK9 siRNA, TRAK2 siRNA, and PCSK9+TRAK2 siRNA groups was higher than in the control group (P < 0.001), with no significant difference in cholesterol efflux between these groups. Cholesterol efflux in the ABCA1 siRNA group was lower than in the control group (P < 0.001); cholesterol efflux in the (PCSK9+ABCA1) siRNA group was lower than in the PCSK9 siRNA group (P < 0.001), and cholesterol efflux in the (TRAK2+ABCA1) siRNA group was lower than in the TRAK2 siRNA group (P < 0.001). These findings indicate that PCSK9 may regulate cholesterol efflux via the TRAK2/ABCA1 pathway.
    Figures and Tables | References | Related Articles | Metrics
    Bioinformatics screening and experimental verification of core genes in chronic myeloid leukemia and imatinib resistance
    Zhou Man, Long Meiting, Xin Guoyan, Huang Mengjun, Yao Zhenglian, Zhao Huajuan, Shen Linqiang, Wu Xijun, Yang Xiaoyan
    2026, 30 (13):  3331-3342.  doi: 10.12307/2026.162
    Abstract ( 38 )   PDF (7814KB) ( 11 )   Save
    BACKGROUND: The origin of chronic myeloid leukemia lies in clonal hematopoietic stem cells, and it is marked by uncontrollable growth of myeloid cells, mostly caused by the BCR-ABL1 fusion gene. Although imatinib has significantly improved patient survival, drug resistance remains a major obstacle to treatment.
    OBJECTIVE: To identify genes associated with imatinib resistance in chronic myeloid leukemia using bioinformatics analysis within the Gene Expression Omnibus database and to explore the mechanisms of resistance.
    METHODS: The present study utilized the Gene Expression Omnibus database, which was created and is currently maintained by the National Center for Biotechnology Information. Two datasets, GSE267522 and GSE174800, were retrieved from the Gene Expression Omnibus database, and each of the two datasets comprised three imatinib-resistant samples and three imatinib-sensitive samples. First, the GEO2R tool was used to screen the differential genes, and the DAVID tool was used to analyze them for Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment. A protein interaction network framework was constructed using the STRING database, and the top 10 hub genes with the highest connectivity values were identified from the network using Cytoscape software. Furthermore, a weighted gene co-expression network analysis algorithm was used to identify key module feature genes. Venn diagram analysis was performed with these genes and the aforementioned 10 hub genes, and the intersection genes were selected as core genes. Finally, a K562 imatinib resistance model was constructed and validated using real-time fluorescence quantitative PCR and western blotting.
    RESULTS AND CONCLUSION: (1) A total of 273 differential genes were screened between the two datasets, of which 81 were downregulated and 192 were upregulated. (2) Gene ontology enrichment analysis revealed that the differential genes were involved in immune response and T-cell receptor signaling. Focusing on the cellular component level, cell components like the outer and inner plasma membranes and cellular exosome showed significant enrichment. Molecular function analysis indicated that the differential genes were involved in interactions between transmembrane receptor proteins and actin. (3) Kyoto Encyclopedia of Genes and Genomes enrichment analysis showed that the differential genes were enriched in the hematopoietic cell lineage, phosphatidylinositol 3-kinase/protein kinase B signaling pathway and cancer pathway. (4) Cytoscape software screened out the top 10 differentially expressed genes by connectivity and intersected them with key module signature genes obtained using a weighted gene co-expression network analysis algorithm. The resulting intersection genes obtained included IRS1, CD52, CD53, CORO1A, KIT, LAPTM5, and PECAM1. (5) The K562 Imatinib resistance beads were successfully constructed. The real-time fluorescence quantitative PCR results showed that compared with the K562 group, the mRNA expression of CD52, CD53, CORO1A, and PECAM1 was significantly increased in the imatinib-resistant K562 group (P < 0.05), while the mRNA expression of IRS1 was significantly decreased (P < 0.05). Furthermore, western blotting revealed increased expression of CD52, CD53, CORO1A, and PECAM1 proteins (P < 0.05), and decreased expression of IRS1 protein (P < 0.05) in the imatinib-resistant K562 strain (consistent with the real-time fluorescence quantitative PCR results). (6) Differences in the expression of K562 imatinib resistance core genes may provide new insights into the mechanisms of imatinib resistance in chronic myeloid leukemia in the future.
    Figures and Tables | References | Related Articles | Metrics
    Effects of basic fibroblast growth factor-loaded composite bioscaffold on angiogenesis of dental pulp stem cells
    Shi Yuxin, Kaiwusail · Tursun, Liu Jia
    2026, 30 (13):  3343-3349.  doi: 10.12307/2026.014
    Abstract ( 34 )   PDF (1350KB) ( 3 )   Save
    BACKGROUND: Previous studies have shown that composite scaffolds prepared from a certain proportion of gelatin-methacryloyl and treated dentin matrix exhibit excellent biological properties, which are beneficial for cell proliferation and adhesion. Composite biological scaffolds loaded with basic fibroblast growth factor provide a new idea for dental pulp revascularization.
    OBJECTIVE: To observe the effect of gelatin-methacryloyl/treated dentin matrix composite biological scaffold loaded with basic fibroblast growth factor on the proliferation, migration, and angiogenic properties of human dental pulp stem cells.
    METHODS: Composite biological scaffolds loaded with 0, 50, 100, 200, and 500 ng/mL of basic fibroblast growth factor were prepared. The proliferation ability of dental pulp stem cells was detected by CCK-8 assay and the optimal mass concentration of basic fibroblast growth factor was screened. The dental pulp stem cells were divided into three groups, namely gelatin-methacryloyl/treated dentin matrix group, basic fibroblast growth factor- gelatin-methacryloyl/treated dentin matrix group, and blank control group. The scratch assay was used to detect the migration ability of dental pulp stem cells. Matrigel tubule formation assay was used to detect the number of branch points of dental pulp stem cell tubules. The immunofluorescence staining was used to detect the expression of vascular endothelial growth factor protein in dental pulp stem cells. qPCR was used to detect the expression of angiogenesis-related genes (vascular endothelial growth factor, transforming growth factor β, and ephrin B2) in dental pulp stem cells.
    RESULTS AND CONCLUSION: (1) CCK-8 assay showed that the gelatin-methacryloyl/treated dentin matrix composite scaffolds loaded with basic fibroblast growth factor could promote the proliferation of dental pulp stem cells at 3 and 5 days of culture, among which the proliferation-promoting effect of basic fibroblast growth factor (100 ng/mL)- gelatin-methacryloyl/treated dentin matrix composite scaffold was the most obvious. (2) Cell scratch assay showed that the cell migration area of basic fibroblast growth factor (100 ng/mL)-gelatin-methacryloyl/treated dentin matrix composite scaffold group was significantly larger than that of gelatin-methacryloyl/treated dentin matrix group and blank control group. (3) Matrigel tubule formation assay showed that the number of branch points of basic fibroblast growth factor (100 ng/mL)-gelatin-methacryloyl/treated dentin matrix composite scaffold was greater than that of gelatin-methacryloyl/treated dentin matrix and blank control groups. (4) Immunofluorescence assay showed that the average positive absorbance value of vascular endothelial growth factor in basic fibroblast growth factor (100 ng/mL)-gelatin-methacryloyl/treated dentin matrix composite scaffold group was higher than that of gelatin-methacryloyl/treated dentin matrix and blank control groups. (5) qPCR assay showed that the expression of vascular endothelial growth factor, transforming growth factor β, and ephrin B2 in the basic fibroblast growth factor (100 ng/mL)-gelatin-methacryloyl/treated dentin matrix composite scaffold group was higher than that in the gelatin-methacryloyl/treated dentin matrix and blank control groups. The results showed that basic fibroblast growth factor (100 ng/mL)-gelatin-methacryloyl/treated dentin matrix composite scaffold exhibited good ability to promote the proliferation, migration, and angiogenesis of dental pulp stem cells.
    Figures and Tables | References | Related Articles | Metrics
    Osteogenic-adipogenic differentiation imbalance of bone marrow mesenchymal stem cells and osteonecrosis of the femoral head: from molecular mechanisms to therapeutic strategies
    Zhang Shilei, Qin Chuanhong, Wang Jianxu, Sun Shui
    2026, 30 (13):  3350-3358.  doi: 10.12307/2026.307
    Abstract ( 51 )   PDF (1319KB) ( 15 )   Save
    BACKGROUND: Osteonecrosis of the femoral head is a common orthopedic condition that can lead to significant disability. A key feature of this disease is the collapse of the femoral head, causing severe hip pain and loss of function. Bone marrow mesenchymal stem cells can differentiate into multiple cell types, including osteoblasts, adipocytes, and chondrocytes. Pathological factors like alcohol and corticosteroids disrupt the balance between osteogenic and adipogenic differentiation. This leads to excessive fat accumulation and reduced bone formation, ultimately contributing to osteonecrosis of the femoral head. 
    OBJECTIVE: To focus on elucidating molecular mechanisms underlying osteonecrosis of the femoral head with a particular focus on the role of bone marrow mesenchymal stem cells, and further discuss the implications of adipocytes.
    METHODS: PubMed was searched for articles published from database inception to June 2025, using “osteonecrosis of the femoral head, bone marrow mesenchymal stem cells, osteogenic differentiation, adipogenic differentiation, bone marrow adipose tissue, adipokines.” Following the inclusion and exclusion criteria, 81 relevant articles were selected for comprehensive analysis.
    RESULTS AND CONCLUSION: A review of research shows that Wnt, transforming growth factor-β/bone morphogenetic protein superfamily, and phosphatidylinositol 3-kinase/protein kinase B signaling pathways, along with various RNA molecules, play a role in regulating the balance between osteogenic and adipogenic differentiation in bone marrow mesenchymal stem cells. These pathways precisely control cell behavior by targeting key transcription factors, such as Runt-related transcription factor 2 for bone formation and peroxisome proliferator-activated receptor γ and CCAAT enhancer binding protein for fat cell development. Furthermore, adipocytes and the signaling molecules they release, such as leptin and adiponectin, can also affect the progression of osteonecrosis of the femoral head through paracrine signaling. This article explains how interactions between bone marrow mesenchymal stem cells and adipocytes contribute to the development of osteonecrosis of the femoral head and, based on current research, suggests potential future interventions and treatment strategies.
    Figures and Tables | References | Related Articles | Metrics
    Analysis of strategies to improve efficiency of in vitro culture of mesenchymal stem cells
    Yang Yuxi, Xu Dan, Liu Zhongshan
    2026, 30 (13):  3359-3369.  doi: 10.12307/2026.339
    Abstract ( 52 )   PDF (1389KB) ( 127 )   Save
    BACKGROUND: The function of mesenchymal stem cells gradually declines as the number of passages increases in the process of in vitro culture, resulting in its limited efficacy in practical clinical application. Nowadays, with the emergence of advanced biotechnology and the substantial improvement of bioengineering materials, a variety of improved strategies have been developed, but there is still no standardized stem cell production standard.
    OBJECTIVE: To summarize the problems that arise during the in vitro culture of mesenchymal stem cells and briefly describe the optimization plan for their in vitro culture.
    METHODS: Using “mesenchymal stem cells, in vitro culture, cell culture, culture conditions, pretreatment, cell senescence” as the Chinese search terms and “mesenchymal stem cells, cell culture, in vitro, culture conditions, preconditioning, cell senescence” as the English search terms, literature published before January 2025 in CNKI and PubMed databases was searched to exclude articles with poor relevance to the topic, long history, and duplication. Finally, 98 articles were included for review.
    RESULTS AND CONCLUSION: (1) This paper summarizes the problems of mesenchymal stem cells in vitro culture, such as cell morphology changes, proliferation and differentiation ability decline, migration and homing ability decline, cell metabolism disorders, and secretion aging related phenotypes. (2) The possible mechanisms of in vitro passage senescence of mesenchymal stem cells, such as genetic material damage, loss of protein homeostasis, intracellular signaling pathways, and changes in the expression of transcription factors, were summarized. (3) Strategies to improve the culture efficiency of mesenchymal stem cells in vitro were summarized, such as genetic engineering to modify stem cells, pharmacological methods to intervene in cell proliferation and differentiation, optimization of stem cell culture environment in vitro, hypoxic preconditioning, and regulation of cytokines. The above research provides a theoretical basis for improving the clinical efficacy of mesenchymal stem cells.
    Figures and Tables | References | Related Articles | Metrics
    Occurrence and development of plant derived extracellular vesicles in the prevention and treatment of musculoskeletal system diseases
    Zhang Yijie, Hong Bowen, Zhou Yi, Shao Yang, Wu Mao, Li Shaoshuo, Wang Jianwei
    2026, 30 (13):  3370-3378.  doi: 10.12307/2026.309
    Abstract ( 86 )   PDF (1441KB) ( 35 )   Save
    BACKGROUND: Plant derived extracellular vesicles have opened up new avenues for the treatment of osteoporosis, osteoarthritis, and cartilage damage due to their unique biological properties and low immunogenicity. 
    OBJECTIVE: To review the research history, extraction and separation methods of plant derived extracellular vesicles, and their application progress in musculoskeletal system diseases. 
    METHODS: Relevant literature published from January 1995 to February 2025 was searched by computer in PubMed, Web of Science, EMbase, China National Knowledge Infrastructure (CNKI), WanFang, and VIP databases using “musculoskeletal system, plant derived extracellular vesicles, exosomes, extracellular vesicle like nanovesicles, osteoporosis, osteoarthritis, wound healing, drug carrier, inflammation” as Chinese and English search terms. Finally, 61 articles were included for analysis.
    RESULTS AND CONCLUSION: The advantages of plant derived extracellular vesicles include relatively simple extraction and purification processes, easy standardization, suitability for large-scale production, lower immunogenicity, greater safety and tolerance, excellent stability, ability to withstand acidic conditions in the stomach and intestines, suitability for oral administration systems, longer in vivo circulation time and tissue-specific targeting, and the ability to cross the blood-brain barrier but not the placental barrier. Plant derived extracellular vesicles have been widely studied in the treatment of osteoporosis, osteoarthritis, promotion of wound healing and blood flow reconstruction, inhibition of inflammatory reactions, and as drug carriers for the treatment of musculoskeletal system diseases.
    Figures and Tables | References | Related Articles | Metrics
    Skeletal muscle-derived exosome-mediated regulation of bone formation and role of exercise intervention
    Lu Biqiong, Wei Zhongjian
    2026, 30 (13):  3379-3391.  doi: 10.12307/2026.340
    Abstract ( 55 )   PDF (2150KB) ( 21 )   Save
    BACKGROUND: Abnormal bone formation is one of the primary causes of increased fracture risk and decreased quality of life. Skeletal muscle, as an important secretory organ, produces skeletal muscle-derived exosomes, which are closely related to bone formation. Recent studies have shown that exercise may regulate bone formation by modulating the secretion of skeletal muscle-derived exosomes. Therefore, a thorough investigation into the role and mechanisms of skeletal muscle-derived exosomes in regulating bone formation is of significant importance for improving quality of life and reducing fracture risk.
    OBJECTIVE: To summarize the role of skeletal muscle-derived exosomes in bone formation and their potential mechanisms, particularly the regulatory effects of exercise intervention on skeletal muscle-derived exosomes, providing new insights for the treatment of abnormal bone formation.
    METHODS: We searched the CNKI and PubMed databases using Chinese and English search terms “exosome, skeletal muscle-derived exosomes, bone formation, osteoblast, exercise.” We screened relevant literature published between database inception and November 2024. Based on the relevance, quality, and suitability of the research content, we ultimately included 81 relevant articles for review.
    RESULTS AND CONCLUSION: (1) Current multi-omics, histological, and molecular biology studies have identified that miR-1, miR-133a, miR-133b, miR-206, and miR-27 in skeletal muscle-derived exosomes, as well as heat shock proteins, insulin-like growth factor binding protein 5, myotilin, and mesoderm paired homeobox protein 2, regulate osteogenic differentiation through the Wnt/β-catenin, bone morphogenetic protein 2 and Runt-related transcription factor 2, and other signaling pathways, improving osteoporosis. (2) Different types, intensities, and durations of exercise interventions have varying effects on the regulation of skeletal muscle-derived exosome release and their role in bone metabolism. However, due to the complexity of in vivo exosome tracking and identification, it is still difficult to precisely identify the source of circulating exosome after exercise. Future research needs to further explore the specific mechanisms. In summary, the role of skeletal muscle-derived exosomes in bone metabolism is increasingly recognized, and exercise intervention, by regulating exosome release, offers new possibilities for the treatment of bone metabolic diseases.
    Figures and Tables | References | Related Articles | Metrics
    Application of exosomes in the diagnosis and monitoring of oral diseases
    Huang Jiayao, Gu Yu
    2026, 30 (13):  3392-3401.  doi: 10.12307/2026.358
    Abstract ( 60 )   PDF (1598KB) ( 16 )   Save
    BACKGROUND: As nanoscale messengers of intercellular communication, exosomes encapsulate miRNAs, proteins, and lipids within vesicles, forming an unique bioinformational code. This can accurately trace the abnormal activity trajectories of diseased cells, providing new approaches for disease diagnosis.
    OBJECTIVE: To briefly describe the basic concepts of exosomes and the regulatory role of related factors in their biogenesis, summarize the current research status of exosomes in oral disease diagnosis, and provide new research directions and a basis for the application of exosomes in the field of stomatology. 
    METHODS: The first author conducted a computerized literature search from January to March 2025 using PubMed, Web of Science, WanFang Data Knowledge Service Platform, and China National Knowledge Infrastructure (CNKI) databases to retrieve relevant literature published between January 2000 and March 2025. The Chinese and English search terms were “exosomes, periodontitis, lichenplanus, oral submucous fibrosis, oral leukemia, oral squamous carcinoma, dental caries, Sjögren syndrome, cleft of lip and/or palate, orthodontics, biomarker.” A total of 76 articles were included for analysis. 
    RESULTS AND CONCLUSION: Exosomes, as a promising class of liquid biopsy biomarkers, have shown notable utility in the diagnosis and monitoring of oral diseases. In oral squamous cell carcinoma research, aberrant expression of miRNAs and proteins in salivary exosomes correlates closely with tumor stage and invasiveness; combining these two biomarkers achieves high sensitivity in diagnosis. For potentially malignant oral lesions, dynamic alterations in exosomal miRNAs mirror the malignant transformation risk of leukoplakia and disease progression in lichen planus. Studies on periodontitis have revealed links between exosomal components and both inflammation severity and treatment response, opening new avenues for non-invasive monitoring. Notably, differential expression of exosomal miRNAs on the mechanically responsive side during orthodontic tooth movement hints at their role in regulating periodontal tissue remodeling. In Sjögren's syndrome, combined detection of ferroptosis-related proteins and miR-1290 in exosomes has surpassed the limitations of traditional biopsy methods. While dental caries research remains in its early stages, investigations into virulence molecules in Streptococcus mutans exosomes and host immune proteins have offered fresh insights for early diagnosis. However, current work is still constrained by challenges such as sample variability, inconsistent technical standards, and gaps in mechanistic understanding. Moving forward, integrating multi-omics approaches, standardizing detection protocols, and advancing exosome-based clinical translation for precision oral disease management will be critical priorities.
    Figures and Tables | References | Related Articles | Metrics
    Exosome loading mode of therapeutic adipose derived stem cells
    Ji Demin, Ma Zhihong
    2026, 30 (13):  3402-3411.  doi: 10.12307/2026.203
    Abstract ( 49 )   PDF (5980KB) ( 45 )   Save
    BACKGROUND: Exosomes secreted by adipose derived stem cells are membrane vesicles with a diameter of 30-150 nm, containing bioactive molecules such as proteins, noncoding RNAs (miRNAs, long noncoding RNAs) and lipids. In recent years, studies have found that exosomes secreted by adipose derived stem cells play a key role in tissue repair, immune regulation, angiogenesis and other pathophysiological processes by mediating intercellular communication. However, the characteristics of exosomes that are easy to be rapidly cleared in the circulatory system limit their clinical application. Optimizing exosome delivery system by developing new loading technology has become an important strategy to improve its therapeutic efficacy.
    OBJECTIVE: To review the research progress of different loading delivery systems of therapeutic adipose stem cell-derived exosomes.
    METHODS: The relevant articles included in CNKI and PubMed were retrieved from database inception to 2025. Chinese and English search terms were “adipose derived stem cells, exosomes, delivery system, hydrogel, metal-organic framework, synthetic polymer scaffolds.” Finally, 50 articles were selected for summary. 
    RESULTS AND CONCLUSION: The stability, targeting and therapeutic efficacy of exosomes have been significantly improved through the innovation of loading materials such as hydrogels, metal organic frameworks and synthetic polymer scaffolds. The biocompatibility of natural hydrogels combined with the environmental responsiveness of smart hydrogels realized the controlled release and precise delivery of exosomes. The synergistic effect of the porous structure of metal organic frameworks and exosomes shows unique advantages in the field of bone regeneration and anti-inflammation. The functional design of synthetic scaffolds provides a biomimetic microenvironment for complex tissue repair. However, current research is still limited to the cell and animal experiment stage, and more experiments are needed to confirm its safety and effectiveness. Future research needs to further optimize the biocompatibility and loading efficiency of materials, explore the synergistic effect of multimodal delivery system, and strengthen the long-term safety evaluation, so as to promote the transition of loading technology of exosomes secreted by adipose derived stem cells from laboratory to clinic, and provide a new paradigm for regenerative medicine and personalized treatment.
    Figures and Tables | References | Related Articles | Metrics
    Exercise-induced extracellular vesicles: action and mechanisms in occurrence and development of insulin resistance
    Yao Lijuan, Wang Yinfeng, Ma Zhennan, Chen Leqin
    2026, 30 (13):  3412-3423.  doi: 10.12307/2026.326
    Abstract ( 37 )   PDF (5031KB) ( 178 )   Save
    BACKGROUND: Extracellular vesicles have emerged as an emerging key mediator of intercellular information exchange. Extracellular vesicles play a key regulatory role in insulin target organs such as skeletal muscle, adipose tissue, and liver by delivering miRNAs, proteins, and lipid molecules. The research on the mechanism of exercise-induced extracellular vesicles in the development of insulin resistance has become a hot frontier in metabolism.
    OBJECTIVE: To sort out the recent research progress between exercise-induced extracellular vesicles and insulin resistance. 
    METHODS: Computerized search of PubMed, MedReading, Web of Science, CNKI, WanFang, and VIP databases was applied, with the time limit of literature published from January 1, 2012 to March 3, 2025, to collect the studies on the effects of extracellular vesicles on diseases under relevant exercise. The search terms in Chinese were “extracellular vesicle, exercise, insulin resistance, disease,” and the search terms in English were “extracellular vesicle, physical exercise, insulin resistance, disease.” Through the inclusion and exclusion criteria, 107 papers were included for review.
    RESULTS AND CONCLUSION: The article systematically comb the relationship between extracellular vesicles, exercise and insulin resistance. The results show that extracellular vesicles, as a key mediator, play an important role in multi-organ metabolic regulation through the delivery of miRNAs, proteins and other molecules to improve insulin resistance, and that different forms of exercise have different impacts on the extracellular vesicles, with aerobic, strength-training, single and high-intensity exercise producing extracellular vesicles showing differential efficacy in insulin resistance. Exercise-induced extracellular vesicles can improve insulin resistance through multi-targets and multi-pathways, as well as have far-reaching effects on insulin signaling pathway, inflammation and overall metabolism regulation, and become a core bridge connecting exercise intervention and metabolism health. Different exercise modes can provide a theoretical basis for the design of precise exercise prescription by reshaping the molecular profile of extracellular vesicles. However, in-depth investigation is still needed to analyze the complex relationship between exercise, extracellular vesicles and insulin resistance, so as to provide systematic theoretical support for the scientific principles of exercise to improve metabolic health, and to open up new ideas and directions for the prevention and therapeutics for obesity, diabetes mellitus and other related metabolic diseases.
    Figures and Tables | References | Related Articles | Metrics
    Gene transfection technology and tissue fibrosis repair
    Wu Xianyuan, Zhang Nini, Huang Guilin
    2026, 30 (13):  3424-3434.  doi: 10.12307/2026.325
    Abstract ( 41 )   PDF (3730KB) ( 15 )   Save
    BACKGROUND: In recent years, studies have found that exosomes have great potential in the field of tissue injury repair. As natural nanoscale vesicle carriers, they have the advantages of low immunogenicity and good biocompatibility, and play an important role in intercellular communication. Engineering cells genetically and enabling them to exert tissue repair functions through paracrine action has become a focus of current researchers.
    OBJECTIVE: To summarize the role of gene transfection technology in the repair of pulmonary, hepatic, cardiac, renal, and salivary gland fibrosis, and to prospect the future research directions and development trends of engineered exosome.
    METHODS: Relevant literature searches were conducted in the PubMed database using keywords such as “gene transfection, gene therapy, transfection, tissue fibrosis, mechanism of fibrosis, radiation-induced salivary gland injury, repair,” and in the CNKI database using keywords such as “gene transfection, gene therapy, tissue fibrosis, fibrosis mechanisms, radiation-induced salivary gland injury, tissue repair.” Through rapid review of article titles and abstracts, articles that were not closely related to the topic were excluded. Finally, 80 articles were selected for review.
    RESULTS AND CONCLUSION: (1) Exogenous genes were introduced into the target cells through genetically engineered stem cells and exosomes derived from genetically engineered stem cells, which can play the role of anti-apoptosis, anti-inflammation and anti-fibrosis, and play an important role in the repair of lung, liver, heart, kidney and salivary gland fibrosis injury diseases. (2) As a natural nano scale intercellular communication carrier, exosomes have gradually become a new carrier for gene therapy due to their excellent biocompatibility, low immunogenicity and high cellular uptake ability. The exosome based on genetic engineering stem cells overcomes the limitations of cell life, low efficiency of cell implantation, and the risk of immune rejection and tumor formation caused by cell transplantation during traditional stem cell transplantation, and has higher safety and more effective targeted delivery ability. (3) The targeted technology of exosomes enhances its targeting by means of genetic engineering and chemical modification, and further improves the therapeutic effect by the separation technology based on microfluidic and interdisciplinary joint treatment strategy. However, at present, there are few studies on the use of genetically engineered cells to play the role of tissue repair through paracrine, and most of them are only based on in vitro experimental studies or in small animal models, lacking large animal models and long-term safety evaluation data. In the future, it is still necessary to strengthen clinical transformation research to further verify its treatment safety and long-term effectiveness.
    Figures and Tables | References | Related Articles | Metrics
    Mesenchymal stem cells and their exosomes in treatment of bronchopulmonary dysplasia
    Huang Jia, Yan Qingyan, Yang Xing, Zhu Xiaoping, Luo Hongfang
    2026, 30 (13):  3435-3445.  doi: 10.12307/2026.143
    Abstract ( 44 )   PDF (3357KB) ( 13 )   Save
    BACKGROUND: Mesenchymal stem cells and their extracellular vesicles can effectively alleviate lung injury, promote lung tissue repair and functional reconstruction through mechanisms such as antioxidant, anti-inflammatory, promoting angiogenesis, and inhibiting pulmonary fibrosis, thereby improving the course and prognosis of neonatal bronchopulmonary dysplasia to a certain extent.
    OBJECTIVE: To review the current research status of mesenchymal stem cells and their extracellular vesicles in neonatal bronchopulmonary dysplasia.
    METHODS: The first author searched articles included in CNKI and PubMed databases. The time limit for literature search was from the establishment of each database to March 2025. “Mesenchymal stem cells, exosomes, bronchopulmonary dysplasia, nanohydrogels, mechanism of action” were used as Chinese and English search terms. Finally, 85 articles that met the criteria were selected for review.
    RESULTS AND CONCLUSION: (1) Mesenchymal stem cells and their extracellular vesicles can mediate various therapeutic mechanisms, including alleviating oxidative stress response, promoting angiogenesis and vascular repair, inhibiting pulmonary fibrosis process, anti-apoptosis, regulating cell autophagy, and participating in immune regulation and inflammation inhibition. Mesenchymal stem cells and their extracellular vesicles have shown good application prospects in the prevention and treatment of neonatal bronchopulmonary dysplasia, and are expected to become one of the important treatment strategies for this disease. (2) Under traditional administration methods, mesenchymal stem cells and their extracellular vesicles are difficult to achieve long-term retention in the lungs, thereby limiting their ability to sustain repair of damaged tissues. In recent years, the introduction of engineering biomaterials such as hydrogels has provided a new solution to this problem. Hydrogel can not only realize the slow release of exosomes in the lung tissue, but also protect them from the influence of the inflammatory microenvironment in the lung to a certain extent, thus improving their biological stability and therapeutic efficacy. Therefore, the hydrogel-based stem cell and exocrine delivery system is expected to become a hot research direction in the treatment of neonatal bronchopulmonary dysplasia in the future.
    Figures and Tables | References | Related Articles | Metrics
    Hot spot and current status of single-cell RNA sequencing in stroke field
    Cao Lifang, Chen Tao, Shou Jiayin, Fan Fangfang
    2026, 30 (13):  3446-3457.  doi: 10.12307/2026.204
    Abstract ( 69 )   PDF (2397KB) ( 147 )   Save
    BACKGROUND: Single-cell RNA sequencing technology has overcome the limitations of traditional sequencing methods in studying cellular heterogeneity and elucidates the dynamic functional changes of neural cells following stroke. Currently, there remains a paucity of comprehensive reviews summarizing the application of single-cell RNA sequencing in stroke research.
    OBJECTIVE: To systematically analyze the recent applications and emerging trends of single-cell RNA sequencing in stroke research to provide a theoretical foundation for advancing prevention and treatment strategies. 
    METHODS: Relevant literature was retrieved from the Web of Science Core Collection using the search query "TS=(stroke) AND TS=(Single-cell sequencing)" with a time span from January 2013 to December 2024. After screening, 160 valid articles were included. Statistical analysis and visualization were conducted using Excel and Citespace 6.4.R2 software, focusing on multiple dimensions including countries, institutions, authors, keywords, and co-cited references.
    RESULTS AND CONCLUSION: Over the past decade, single-cell RNA sequencing applications in stroke research have shown consistent growth, culminating in a peak of 64 publications in 2024. China (98 articles) and the United States (50 articles) emerged as leading research forces, though China exhibits lower betweenness centrality in international research collaboration compared to the United States, suggesting enhanced transnational cooperation is required to improve global influence. Key institutions including Capital Medical University, Shanghai Jiao Tong University, and Stanford University have formed research teams led by principal investigators Zhang Jianmin, Lu Jianan, and Li Huaming, focusing on microglial heterogeneity and neurovascular unit dysfunction. Keyword analysis revealed that microglial activation-associated neuroinflammation, neuronal apoptosis, and angiogenesis constitute major research hotspots in stroke mechanisms, while molecular docking combined with single-cell RNA sequencing integrated analysis has emerged as a novel paradigm for targeted stroke drug discovery. Co-citation analysis identified transcriptional characteristics of pro-inflammatory and repair-oriented microglial subpopulations through single-cell RNA sequencing, along with their regulatory mechanisms on inflammation and apoptosis via the tumor necrosis factor-α/interleukin-6 signaling pathway. These findings indicate that single-cell RNA sequencing technology has elucidated novel mechanisms in stroke pathogenesis through decoding cellular heterogeneity, while the integration with molecular docking analysis has accelerated high-throughput screening of targeted therapeutic agents. Future integration with spatial omics and artificial intelligence may overcome current limitations of single-cell RNA sequencing, thereby providing robust research tools for developing innovative therapeutic strategies against stroke.
    Figures and Tables | References | Related Articles | Metrics
    Identification of diagnostic biomarkers related to osteoporosis exosomes and preliminary drug screening
    Liang Zhou, Pan Chengzhen, Chen Feng, Zhang Chi, Yang Bo, Wei Zongbo, Meng Jianhua, Zhou Zhu
    2026, 30 (13):  3458-3473.  doi: 10.12307/2026.324
    Abstract ( 50 )   PDF (13542KB) ( 5 )   Save
    BACKGROUND: In recent years, exosomes, as key mediators of intercellular communication, have played important roles in the occurrence, progression, and treatment of osteoporosis. The active molecules they carry, such as miRNAs and proteins, can regulate the functions of osteoblasts and osteoclasts and affect bone metabolic balance. However, the specific mechanisms still require further research.
    OBJECTIVE: To identify and validate core exosomal genes in osteoporosis, explore their immune regulatory mechanisms, and predict potential targeted drugs using 4D-DIA proteomics, multiple machine learning algorithms, and Mendelian randomization analysis, providing new insights for mechanistic research and precision treatment of osteoporosis.
    METHODS: Twelve Sprague-Dawley rats were divided into two groups: sham surgery group and osteoporosis model group, with 6 rats in each group. After model establishment by ovariectomy, femoral tissue samples of rats were collected for 4D-DIA proteomic analysis to identify differentially expressed genes, along with Weighted Gene Co-expression Network Analysis. Expression profiles GSE56815 and GSE7158 were collected from the GEO database as validation datasets. Exosome-related genes were downloaded from the GeneCards database. The intersections of these genes with Weighted Gene Co-expression Network Analysis module genes from proteomics and differentially expressed genes from validation datasets were used to obtain osteoporosis-exosome related genes. Functional enrichment analysis was performed. Subsequently, three machine learning algorithms - Random Forest, LASSO, and support vector machine - were used to screen feature genes separately, and their intersection was taken to obtain osteoporosis-exosome core genes. A prediction model was further established and the receiver operating characteristic curve was verified. CIBERSORT was used for immune infiltration analysis to examine the differential expression of immune cell subpopulations in osteoporosis. Single-sample gene set enrichment analysis was used to analyze the correlation between osteoporosis-exosome core genes and immune cell subpopulations, and simultaneously analyze the relevant biological pathways of the core genes. StarBase database was applied to predict the RNA Binding Protein regulatory network of osteoporosis-exosome core genes. Finally, two-sample Mendelian randomization was employed to verify the causal relationship between exosome core genes and osteoporosis. Drug enrichment analysis was conducted through DSigDB database. Molecular docking visualization was performed using the CB-DOCK2 website. 
    RESULTS AND CONCLUSION: (1) 4D-DIA proteomics identified 1 322 differential proteins related to osteoporosis. Through Weighted Gene Co-expression Network Analysis, two characteristic modules containing 402 genes were identified. The Gene Cards database curated 878 exosome-related genes. Differential analysis of the GEO validation dataset identified 4 447 differential proteins. The intersection of these three gene sets yielded 31 genes associated with osteoporosis and exosomes. (2) Functional enrichment analysis of the related genes indicated that they were primarily associated with neutrophil extracellular trap formation, the Rap1 signaling pathway, and focal adhesions. (3) Three machine learning algorithms identified four core genes related to osteoporosis and exosomes, among which two genes (ITGB3 and SERPINA1) exhibited consistent differential expression in both animal models and the GEO validation dataset. The receiver operating characteristic curve showed that ITGB3 and SERPINA1 exhibited high area under the curve values in both the animal models and the GEO validation dataset. Models constructed with either individual genes or a combination of the two genes achieved area under the curve values greater than 0.9. (4) Immune infiltration gene set enrichment analysis revealed that the high expression of ITGB3 and SERPINA1 was positively correlated with M1 macrophages. High expression of ITGB3 and SERPINA1 was also associated with the NOD-like receptor signaling pathway. (5) The RNA Binding Protein regulatory network showed that ITGB3 and SERPINA1 jointly regulated 10 RNA-binding proteins, including HNRNPC, G3BP1, EIF3D, CTCF, U2AF2, and MDTH. (6) Two-sample Mendelian randomization analysis indicated that SERPINA1 exerted an inhibitory effect on osteoporosis, making it a protective factor against osteoporosis. (7) Drug enrichment analysis of SERPINA1 identified 36 drugs with a P-value < 0.05. Molecular docking revealed that 9 of these drugs had binding energies lower than -29.4 kJ/mol, with β-carotene exhibiting the strongest binding energy to SERPINA1 (-35.28 kJ/mol). The above findings confirm that ITGB3 and SERPINA1 are core genes associated with osteoporosis-exosomes. Both genes play a critical role in disease progression by participating in specific immune processes and regulating the NOD-like receptor signaling pathway. These genes exhibit precise predictive potential for the diagnosis of osteoporosis.
    Figures and Tables | References | Related Articles | Metrics
    Natural killer cells in treatment of prostate cancer: a bibliometric analysis from basic research to clinical applications
    Jiang Linglong, Zhang Yuan, Shen Yuwei, Pan Jiawei, Sun Yangyang, Zhu Jundong, Fan Min, Shi Jian
    2026, 30 (13):  3474-3484.  doi: 10.12307/2026.120
    Abstract ( 47 )   PDF (2908KB) ( 11 )   Save
    BACKGROUND: Natural killer cells have shown promising clinical applications in tumor immunotherapy in recent years, and the use of natural killer cells for the treatment of prostate cancer has attracted increasing attention. However, there is currently a lack of bibliometric analysis in this field. 
    OBJECTIVE: To conduct a visual analysis of the research field of natural killer cell therapy for prostate cancer using software such as CiteSpace and VOS viewer.
    METHODS: The English documents are based on the Web of Science Core Collection database constructed by Clarivate Analytics and the PubMed database developed by the National Center for Biotechnology Information (NCBI), which is affiliated with the National Library of Medicine (NLM). We performed a visual analysis of the annual distribution, countries, authors, institutions, journals, and keywords of articles published over the past 10 years (2015–2025) using CiteSpace, VOS viewer, and Bibliometric websites. This analysis aimed to investigate the hotspots and trends in this research field.
    RESULTS AND CONCLUSION: A total of 684 eligible studies were included in the analysis. The overall publication trend showed slight fluctuations but generally increased. According to the statistical results, the United States had the highest number of English-language publications. The author with the highest number of publications was Chen Y from the Memorial Sloan Kettering Cancer Center, with a total of 12 articles. The author with the highest number of citations was Zhang L from the Department of Physiology and Biophysics at the Zilkha Neurogenetic Institute, with a total of 629 citations. The top three institutions in terms of English-language publications were National Institutes of Health, Memorial Sloan Kettering Cancer Center, and University of California. The top three high-frequency keywords were Expression, Tumor microenvironment, and Activation. These results indicate that research on natural killer cells in the field of prostate cancer treatment has gradually increased over the past decade. Analysis of keywords and emerging terms reveals that the research hotspots in the field of natural killer cell therapy for prostate cancer are from enhancing the proliferation and cytotoxicity of natural killer cells, and the interactions between immune cells and natural killer cells to the inhibitory effects of the tumor microenvironment on natural killer cells. The research direction of natural killer cells in the treatment of prostate cancer has shifted from the initial killing and inhibitory mechanism of natural killer cells on tumor cells and enhancing the proliferation ability and cytotoxicity of natural killer cells to improving the immunotherapeutic effect of natural killer cells and the immunosuppressive effect of the tumor microenvironment on natural killer cells by regulating gene expression. How to improve the targeting and killing effects of natural killer cells is the treatment focus in this field.
    Figures and Tables | References | Related Articles | Metrics