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18 February 2026, Volume 30 Issue 5 Previous Issue   

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Postmenopausal osteoporosis: predictive values of muscle mass, grip strength, and appendicular skeletal muscle index Yang Zhijie, Zhao Rui, Yang Haolin, Li Xiaoyun, Li Yangbo, Huang Jiachun, Lin Yanping, Wan Lei, HuangHongxing 2026, 30 (5):  1073-1080.  doi: 10.12307/2026.039 Abstract ( 65 )   PDF (1165KB) ( 19 )   Save BACKGROUND: The prevalence of osteoporosis is high in postmenopausal women, but muscle mass, grip strength, and how these factors affect osteoporosis are understudied, and the exact link between them has not been clarified. OBJECTIVE: To investigate the correlation between muscle mass, grip strength, appendicular skeletal muscle index and bone mineral density in postmenopausal women with osteoporosis and to assess the potential values of these indices in predicting and diagnosing postmenopausal osteoporosis. METHODS: Eighty-three postmenopausal women were collected from the outpatient clinic of the Third Affiliated Hospital of Guangzhou University of Chinese Medicine from February 2023 to January 2024. General data were collected. Bone mineral density was detected. T-value, muscle mass of each part, grip strength were recorded. The body mass index and appendicular skeletal muscle index were calculated. The patients were categorized into non-osteoporosis group (n=17) and postmenopausal osteoporosis group (n=66) according to T value and fracture history, and were statistically analyzed accordingly. RESULTS AND CONCLUSION: (1) The body mass, body mass index, bone mineral density of the overall lumbar spine, muscle mass and appendicular skeletal muscle index were higher in the non-osteoporosis group than the osteoporosis group (P < 0.05). (2) Muscle mass was positively correlated with bone mineral density of the overall lumbar spine and individual vertebrae (P < 0.05). (3) Multiple stepwise linear regression analysis showed that body mass and grip strength were linearly and positively correlated with muscle mass; body height and muscle mass were linearly and positively correlated with grip strength, and body mass was linearly and negatively correlated with grip strength. Body mass index was linearly and positively correlated with bone mineral density, and age was linearly and negatively correlated with bone mineral density. (4) Analysis by receiver operating characteristic curve showed that: muscle mass (the area under the curve, sensitivity, specificity and critical value of muscle mass were 0.744, 76.50%, 74.20% and 36.50 kg, respectively, with P=0.002) and appendicular skeletal muscle index (the area under the curve, sensitivity, specificity and critical value of appendicular skeletal muscle index were 0.739, 82.40%, 62.10% and 5.81 kg/m2, respectively, and P=0.002) had good predictive value for postmenopausal osteoporosis. To conclude, a reduction in muscle mass and appendicular skeletal muscle index can help to predict the risk of postmenopausal osteoporosis, and the possibility of osteoporosis should be taken into account in postmenopausal women when muscle mass is < 36.50 kg or appendicular skeletal muscle index is < 5.81 kg/m2, in order to prevent the occurrence of postmenopausal osteoporosis. Figures and Tables | References | Related Articles | Metrics

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Effects of resistance training on quadriceps mass and knee joint function in patients with osteoporosis and sarcopenia Zhou Jian, Zhang Tao, Zhou Weili, Zhao Xingcheng, Wang Jun, Shen Jie, Qian Li, Lu Ming 2026, 30 (5):  1081-1088.  doi: 10.12307/2026.001 Abstract ( 62 )   PDF (1341KB) ( 21 )   Save BACKGROUND: The quadriceps strength of patients with osteoporosis and sarcopenia is significantly reduced, which can further reduce the function of the knee joint, affect the function of the lower limbs and even lead to a decrease in whole-body coordination. It is speculated that a reasonable quadriceps training program and personalized guidance are beneficial to the recovery of knee joint function in patients with osteoporosis and sarcopenia. OBJECTIVE: To observe the effect of short-term moderate-intensity resistance rehabilitation training on the mass and function of the quadriceps and knee joint function in patients with osteoporosis and sarcopenia.  METHODS: Using the integrated physical examination and rehabilitation model, 375 patients with osteoporosis and sarcopenia were screened at the Health Management Center of Shanghai Public Health Clinical Center. They underwent 12 weeks of combined/comprehensive exercise rehabilitation based on resistance exercise, including quadriceps resistance isotonic and isometric contraction training twice a week (3-5 sets each time, 10-15 minutes per set) and aerobic exercise/balance exercise two or three times a week (30 minutes each time). Assessments and data collection were performed before rehabilitation training, 12 weeks after rehabilitation training, and at follow-up 12 weeks after stopping rehabilitation training, mainly including knee joint range of motion and proprioception, quadriceps muscle strength, and cross-sectional area (magnetic resonance imaging results), pain, knee joint function (Hospital for Special Surgery score) and walking function (“up-and-go” time and 6 m pace test results) as well as the patient's psychological status assessment.   RESULTS AND CONCLUSION: All 375 patients completed 12 weeks of rehabilitation training and 12 weeks of follow-up without any adverse events. (1) Compared with before training, the patients’ gait speed and knee range of motion increased significantly after 12 weeks of rehabilitation training (P < 0.01), the time of “stand-to-walk” decreased (P < 0.01), and the proprioception of the knee joint and the strength of the quadriceps femoris were significantly improved (P < 0.01); and at the follow-up visit 12 weeks after stopping training, the above indicators and functions of the patients were well maintained (P > 0.05). (2) Magnetic resonance imaging results showed that the effective cross-sectional area of the quadriceps femoris did not improve significantly after 12 weeks of rehabilitation training (P > 0.05); but the Hospital for Special Surgery score of knee joint function increased significantly (P < 0.01), and the visual analog pain scale score decreased significantly (P < 0.01), suggesting that this may be related to the improvement of quadriceps femoris quality by resistance rehabilitation training. (3) The results of the Hospital Anxiety and Depression Scale score showed that the anxiety and depression scores of the patients continued to decrease, both at 12 weeks of rehabilitation training and at 12 weeks after stopping training (P < 0.01). It is suggested that resistance rehabilitation training of the quadriceps can help patients with osteoporosis and sarcopenia to restore quadriceps muscle strength, increase range of motion, improve proprioception and joint stability, thereby enhancing knee joint function, reducing pain, improving depression and anxiety, and to a certain extent promoting the coordinated recovery of the musculoskeletal system. Figures and Tables | References | Related Articles | Metrics

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Effects of long-term endurance exercise on kl/FGF23 axis and calcium-phosphorus metabolism in naturally aging mice Peng Tuanhui, Song Hongming, Yang Ling, Ding Xiaoge, Meng Pengjun 2026, 30 (5):  1089-1095.  doi: 10.12307/2026.042 Abstract ( 63 )   PDF (860KB) ( 20 )   Save BACKGROUND: Studies have shown that disorders of mineral metabolism may be responsible for premature aging and that the kl/FGF23 axis plays an important role in mineral metabolism. OBJECTIVE: To explore the effect of long-term endurance exercise on the kl/FGF23 axis in naturally aging mice, and to observe the impact of long-term endurance exercise on calcium and phosphorus metabolism, so as to provide a reference for the influence of long-term endurance exercise on natural aging. METHODS: Twenty-two 5-week-old SPF male balb/c mice were randomly divided into three groups: young and quiet control group, natural aging quiet group and natural aging exercise group. Mice in the young and quiet control group were then killed immediately. Mice in the natural aging quiet group were raised normally until 60 weeks of age. Mice in the natural aging exercise group were subjected to adaptive exercise for 1 week, followed by the maximum running speed test. The official exercise speed was set at 70% of the maximum running speed, and exercise was performed on Mondays, Wednesdays, and Fridays for 50 minutes each. Maximum running speed was retested at 8-week intervals to adjust the official exercise speed until the age of 60 weeks. (3) Enzyme-linked immunoassay was used to measure the levels of femoral fibroblast growth factor 23, renal fibroblast growth factor receptor 1, 1α-hydroxylase, and serum 1,25(OH)2D3. RESULTS AND CONCLUSION: (1) Compared with the young and quiet control group, serum calcium and phosphorus levels in natural aging quiet group had no significant changes (P > 0.05), but bone calcium and phosphorus levels were significantly reduced (P < 0.01). Compared with the natural aging quiet group, the serum phosphorus level was significantly reduced (P < 0.05), the serum calcium level did not change (P > 0.05), and bone calcium and phosphorus levels were significantly increased in the natural aging exercise group (P < 0.05). (2) Compared with the young and quiet control group, the level of fibroblast growth factor 23 in the femur of the natural aging quiet group was significantly increased (P < 0.05). Compared with the natural aging quiet group, the level of fibroblast growth factor 23 in the femur of the natural aging exercise group was reduced, but it was not statistically significant (P > 0.05). (3) Compared with the young and quiet control group, the renal Klotho protein expression, the renal fibroblast growth factor receptor 1, 1α-hydroxylase, and serum 1, 25(OH)2 D3 levels in the natural aging quiet group were significantly decreased (P < 0.05, P < 0.01). Compared with the natural aging quiet group, the levels of the above-mentioned indicators were significantly increased in the natural aging exercise group (P < 0.05, P < 0.01). To conclude, long-term endurance exercise can regulate Klotho protein and fibroblast growth factor 23 through the kl/FGF23 axis, thereby affecting the expression of 1α-hydroxylase and the level of 1,25(OH)₂D₃, and further regulating the body's calcium and phosphorus metabolism, especially phosphate metabolism. This indicates that long-term endurance exercise can delay the natural aging of the body through the kl/FGF23 axis. Figures and Tables | References | Related Articles | Metrics

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Weighted gene co-expression network analysis combined with machine learning to screen and validate biomarkers for osteoarthritis Zhang Qian, Huang Dongfeng 2026, 30 (5):  1096-1105.  doi: 10.12307/2026.021 Abstract ( 58 )   PDF (3474KB) ( 38 )   Save BACKGROUND: Dyslipidemia affects chondrocyte metabolism and plays an important role in the occurrence and progression of osteoarthritis, yet its underlying mechanisms remain unclear. OBJECTIVE: To identify characteristic genes related to lipid metabolism in chondrocytes of osteoarthritis through the weighted gene co-expression network analysis combined with machine learning algorithms and to conduct the preliminary experimental validation. METHODS: Based on the weighted gene co-expression network analysis and linear models for microarray data, differentially co-expressed genes were identified. Machine learning methods were used for screening characteristic genes related to lipid metabolism. Protein-protein interaction analysis was conducted to explore the interaction network and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were employed to investigate the signaling pathways involved in the differentially co-expressed genes. Subsequently, immune correlation analysis was utilized to identify the associations between the characteristic genes and immune infiltration patterns. Furthermore, in vitro molecular experiments were performed to validate the mRNA and protein levels of the characteristic genes.  RESULTS AND CONCLUSION: (1) A total of 123 high-expression and 110 low-expression differentially co-expressed genes were identified after data normalization and application of principal component analysis, weighted gene co-expression network analysis, and linear models for microarray data. (2) Thirty-seven characteristic genes were screened using logistic regression, random forest, and support vector machine, among which SMPD3 and CYP4F3 were identified as two characteristic genes related to lipid metabolism. (3) Protein-protein interaction analysis revealed that SMPD3 and CYP4F3 proteins showed relatively low levels of interaction. (4) Gene Ontology analysis indicated that these genes were primarily enriched in multiple biological processes, including neutrophils and their immune responses, immune system processes, and neutrophil activation. Kyoto Encyclopedia of Genes and Genomes enrichment analysis suggested that they were mainly involved in key pathways such as extracellular matrix-receptor interaction and cell adhesion. (5) Cell type Identification by estimating relative subsets of RNA transcripts immune infiltration analysis showed significant differences in eight types of immune cells in osteoarthritis. Further correlation analysis revealed that SMPD3 was significantly positively correlated with resting dendritic cells (r=0.44, P=3.6×10-3) and significantly negatively correlated with neutrophils (r=-0.48, P=1.7×10-3), whereas CYP4F3 was significantly positively correlated with monocytes and neutrophils (r=0.76, P=7.6×10-9; r=0.73, P=6.0×10-8), and significantly negatively correlated with T follicular helper cells and resting dendritic cells (r=-0.38, P=0.01; r=-0.38, P=0.01). (6) In vitro molecular experiments demonstrated that SMPD3 mRNA and protein levels were significantly increased in the osteoarthritis group, while CYP4F3 mRNA and protein levels were decreased. To conclude, the lipid metabolism-related SMPD3 and CYP4F3 of osteoarthritis can serve as potential biomarkers for the targeted therapy of osteoarthritis and for assessing cartilage repair or degeneration, which provides a new strategy for exploring the relationship between dyslipidemia and osteoarthritis and for clinical targeted treatment in Chinese population. Figures and Tables | References | Related Articles | Metrics

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Effect and mechanism of peroxiredoxin 1 in microglial inflammation after spinal cord injury Yin Yongcheng, Zhao Xiangrui, Yang Zhijie, Li Zheng, Li Fang, Ning Bin 2026, 30 (5):  1106-1113.  doi: 10.12307/2026.035 Abstract ( 50 )   PDF (1215KB) ( 30 )   Save BACKGROUND: The inflammatory response of microglia is closely related to neuronal survival, regeneration, and functional recovery after spinal cord injury. Peroxiredoxin 1 is not only involved in the regulation of oxidative stress, but also has an important effect on cell proliferation, apoptosis, and inflammatory response. OBJECTIVE: To investigate the role and mechanism of peroxiredoxin 1 in the inflammatory response of microglia following spinal cord injury. METHODS: (1) Twelve female C57BL/6 mice were randomly divided into sham-operated (n=6) and spinal cord injury (n=6) groups. The sham-operated group was not modeled and acute spinal cord injury models were constructed in the spinal cord injury group using the modified Allen’s method. Spinal cord tissue at the injured site was taken at 7 days after modeling and transcriptome sequencing was performed to identify differentially expressed genes. The expression of peroxiredoxin 1 in spinal cord tissues was verified using western blot and RT-qPCR. (2) Mouse microglia BV2 were divided into two groups: the control group was stimulated with lipopolysaccharide for 6 hours, and in the knockout group, lipopolysaccharide stimulation was applied for 6 hours at 24 hours after peroxiredoxin 1 was knocked down in the cells. RT-qPCR was performed to detect mRNA expression of peroxiredoxin 1, inflammatory factors (interleukin 1β, interleukin 6, inducible nitric oxide synthase, tumor necrosis factor α, C-C motif chemokine ligand 2, and C-X-C motif chemokine ligand 2), and western blot was performed to detect the expression of peroxiredoxin 1, inducible nitric oxide synthase, and reactive oxygen/ mitogen-activated protein kinase signaling pathway proteins. Mouse microglia BV2 were treated in two groups: the control group was stimulated by hydrogen peroxide for 4 hours, and the knockout group was stimulated by hydrogen peroxide for 4 hours at 24 hours after knockdown of peroxiredoxin 1. The level of reactive oxygen species was detected by 2,7-dichlorodihydrofluorescein diacetate probe. RESULTS AND CONCLUSION: (1) Results from transcriptome sequencing, western blot and RT-qPCR confirmed that peroxiredoxin 1 expression levels in mouse spinal cord tissues were significantly higher in the spinal cord injury group than the sham-operated group (P < 0.05). (2) Peroxiredoxin 1 knockdown in microglial cells led to decreased expression of peroxiredoxin 1 mRNA and protein (P < 0.05), increased mRNA expression of interleukin 1β, interleukin 6, inducible nitric oxide synthase, tumor necrosis factor α, C-C motif chemokine ligand 2, and C-X-C motif chemokine ligand 2 (P < 0.05), increased protein expression of inducible nitric oxide synthase, P-P38, P-JNK and P-ERK proteins (P < 0.05), and increased level of reactive oxygen species (P < 0.05). To conclude, peroxiredoxin 1 regulates microglial inflammation by targeting the reactive oxygen species/mitogen-activated protein kinase signaling pathway. Figures and Tables | References | Related Articles | Metrics

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Forskolin promotes C2C12 myoblast differentiation via regulating the ERK and Akt signaling pathways Huang Liuyan, Zhang Wenxi, Chen Shuwen, Yu Shimei, Dai Zhong, Zuo Changqing 2026, 30 (5):  1114-1121.  doi: 10.12307/2026.024 Abstract ( 60 )   PDF (1582KB) ( 36 )   Save BACKGROUND: Forskolin, a diterpenoid natural compound extracted from Coleus forskohlii, has a crucial regulatory role in skeletal muscle repair. However, the regulatory role of forskolin on myogenic differentiation of C2C12 skeletal muscle cells has not been fully explored. OBJECTIVE: To explore the effects of forskolin on the differentiation of C2C12 myoblast cell line and probe into the underlying molecular mechanisms. METHODS: C2C12 cells were treated with 0, 0.1, 0.25, 0.5, 1, 5, 10 and 20 μmol/L forskolin during growth, and cell proliferation was detected by cell counting kit-8 and qRT-PCR. C2C12 cells were treated with 0, 0.25, 0.5 and 1 μmol/L forskolin during the induction of myogenic differentiation. Immunofluorescence staining and qRT-PCR were used to detect C2C12 cells differentiation. Western blot was used to detect the expression level of myogenic differentiation-related signaling pathway proteins. RESULTS AND CONCLUSION: (1) The viability of C2C12 cells was decreased and cell proliferation was inhibited after treatment with high concentrations (> 1 μmol/L) of forskolin. (2) The qRT-PCR results showed that forskolin up-regulated the expression of Myh2, Myh4, Myomaker, but down-regulated the expression of Myh7 compared with the 0 μmol/L group, when C2C12 cells were differentiated for 4 days. Immunofluorescence staining results showed that the fusion index and myotube diameter of C2C12 cells were increased after forskolin treatment, and the number of myotubes was also increased. (3) Western blot results showed that the phosphorylated extracellular signal-regulated kinase 1/2 expression was inhibited; however, the phosphorylated protein kinase B was promoted after treatment with forskolin. The protein expression level of the myogenic differentiation transcription factor Myogenin was significantly up-regulated after treatment with forskolin. The above results demonstrate that forskolin may promote myogenic differentiation of C2C12 skeletal muscle cells through the extracellular signal-regulated kinase 1/2 and protein kinase B signaling pathway. Figures and Tables | References | Related Articles | Metrics

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Effects of ammonia poisoning on cognitive behavior and hippocampal synaptic damage in mice Zhang Jiuxuan, Zhang Jinnan, Sui Xiaofan, Pei Xiaxia, Wei Jianhong, Su Qiang, Li Tian 2026, 30 (5):  1122-1128.  doi: 10.12307/2026.044 Abstract ( 51 )   PDF (1232KB) ( 9 )   Save BACKGROUND: Ammonia poisoning is considered to be the main hypothesis for the pathogenesis of hepatic encephalopathy. Ammonia can lead to psychiatric and cognitive behavioral disorders, although the specific pathological molecular mechanisms remain unclear.  OBJECTIVE: To investigate the effects of ammonia poisoning on cognitive behavior and hippocampal neuronal synapses in mice.  METHODS: Thirty-two C57BL/6J mice were randomly divided into a normal control group and an ammonium chloride group, with 16 mice in each group. Normal saline was injected intraperitoneally in the control group, and ammonium chloride (10 mmol/kg) was injected intraperitoneally in the ammonium chloride group to construct a model of ammonia poisoning, once a day. After 7 days of ammonium chloride intervention, blood samples were collected from the hearts of six mice in each group for blood ammonia concentration detection. Behavioral experiments, including the open field test, novel object recognition test, and Y-maze test, were performed to assess mental and cognitive-behavioral changes in mice. Finally, hippocampal tissues were extracted for western blot analysis to detect the expression levels of synaptophysin and postsynaptic density protein-95 in hippocampal neurons.  RESULTS AND CONCLUSION: The blood ammonia concentration was significantly elevated in the ammonium chloride group compared with the control group (P < 0.05). Mice in the ammonium chloride group showed anxiety-like behavior and disinhibition phenomenon, and a significant decrease in recognition memory and working memory ability. Western blot results revealed that the expression of synaptophysin and postsynaptic density protein-95 protein in hippocampal neurons in the ammonium chloride group was lower than that in the control group (P < 0.05). To conclude, ammonia poisoning can induce hippocampal neuronal synaptic damage, leading to psychiatric and cognitive behavioral abnormalities in mice. Figures and Tables | References | Related Articles | Metrics

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Autophagy-related gene expression in pulmonary fibrosis models: bioinformatic analysis and experimental validation Liu Kexin, , Hao Kaimin, Zhuang Wenyue, , Li Zhengyi 2026, 30 (5):  1129-1138.  doi: 10.12307/2026.040 Abstract ( 59 )   PDF (2814KB) ( 29 )   Save BACKGROUND: The stress effect of autophagy on epithelial cells, fibroblasts and myofibroblasts is closely related to the formation process of pulmonary fibrosis. OBJECTIVE: To screen the genes related to autophagy in patients with pulmonary fibrosis, and explore their correlation with the prognosis of patients with pulmonary fibrosis, in order to provide a new target for clinical intervention in pulmonary fibrosis. METHODS: The gene expression profiling dataset downloaded from GSE70866 was used as a training set, differentially expressed genes between pulmonary fibrosis patients and normal healthy individuals was analyzed using the R language and intersected with autophagy-related genes to identify the differentially expressed genes with the most significant changes. Multiple analysis methods were used to identify key prognostic genes and construct genetic prognostic models. Patients with pulmonary fibrosis were divided into high-risk and low-risk groups according to their risk scores, and the validity of the prognostic model was verified using the Siena cohort and Leuven cohort validation sets. A cell model of pulmonary fibrosis was established by inducing HFL-1 cells (human embryonic lung fibroblasts) with transforming growth factor-β1, and an animal model of pulmonary fibrosis was established in mice by tracheal instillation of bleomycin to validate the expressions of prognostic genes. RESULTS AND CONCLUSION: (1) There were 2 650 differentially expressed genes between fibrotic tissue and normal tissue. Among them, 34 genes related to autophagy showed significant expression changes. (2) Kaplan-Meier survival analysis curves for the Siena cohort and Leuven cohort validation sets showed significantly lower survival in the high-risk group than in the low-risk group. (3) Three autophagy genes related to prognosis were screened out: myelocytomatosis viral oncogene (MYC), C-C motif chemokine ligand 2 (CCL2), and GABA type a receptor associated protein like 1 (GABARAPL1). (4) Both in vivo and in vitro studies showed that compared with the control group, the expression levels of myelocytomatosis viral oncogene and C-C motif chemokine ligand 2 mRNA and protein were significantly higher in the lung fibrosis model group (P < 0.01, P < 0.05), while the expression levels of GABA type a receptor associated protein like 1 mRNA and protein were lower (P < 0.001). To conclude, bioinformatics methods are used to analyze the expression of three autophagy-related genes in pulmonary fibrosis and their correlation with the prognosis of patients with pulmonary fibrosis. The constructed prognostic model has good predictive ability for the 1-, 2-, and 3-year survival rates of patients with pulmonary fibrosis. Moreover, in vivo and in vitro models have been used to verify that myelocytomatosis viral oncogene and C-C motif chemokine ligand 2 are highly expressed in lung fibroblasts and tissues, and that GABA type a receptor associated protein like 1 is lowly expressed. Figures and Tables | References | Related Articles | Metrics

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Mechanism of depression-like behavior in chronic social defeat stress mice based on high-throughput sequencing Zhang Di, Zhao Jun, Ma Guangyue, Sun Hui, Jiang Rong 2026, 30 (5):  1139-1146.  doi: 10.12307/2026.041 Abstract ( 42 )   PDF (1746KB) ( 33 )   Save BACKGROUND: Stress-induced damage to hippocampal neurons may underlie abnormalities in neuronal structure and function, ultimately leading to mood disorders. G protein-coupled receptors in brain tissue play an important role in mood regulation. OBJECTIVE: To analyze the mechanism of depression-like behavior in chronic social defeat stress mice based on high-throughput sequencing and bioinformatics analysis.  METHODS: C57BL/6J mice were randomly divided into control group and model group. There was no special treatment in the control group, while a mouse model of chronic social defeat stress was established in the model group. Depression-like behavior was assessed through the sucrose preference test, tail suspension test, and forced swim test. Anxiety behavior was evaluated using the elevated plus-maze, while social behavior was measured through the social interaction test. Cognitive function was assessed with the Y-maze spontaneous alternation test. Immunofluorescence staining was performed to quantify microglia markers in the mouse hippocampus, and Nissl staining was used to examine neuronal damage in mice. High-throughput sequencing was used to identify differentially expressed genes and gene enrichment in the mouse hippocampus, and qPCR was used to measure the expression of G protein-coupled receptors in the mouse hippocampus. RESULTS AND CONCLUSION: (1) Compared with the control group, chronic social defeat stress mice showed significant behavioral impairments, including increased anxiety, depression, and cognitive deficits. (2) Additionally, the Nissl body light density in hippocampal neurons was significantly reduced in chronic social defeat stress mice. (3) Sequencing results revealed synaptic damage in the neurons after chronic social defeat stress. Microglia activation was also markedly increased in the hippocampus of CSDS mice. Furthermore, the expression of G protein-coupled receptors in the hippocampus was significantly higher in chronic social defeat stress mice compared with the control group. These findings suggest that chronic social defeat stress induces anxiety, depression, and cognitive deficits in mice, accompanied by neuropathological changes in the hippocampus, and that altered G protein-coupled receptors expression may play a key role in these behavioral and neuropathological changes. Figures and Tables | References | Related Articles | Metrics

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Autophagy regulates early embryonic development in mice via affecting H3K4me3 modification Hu Jing, Zhu Ling, Xie Juan, Kong Deying, Liu Doudou 2026, 30 (5):  1147-1155.  doi: 10.12307/2026.022 Abstract ( 54 )   PDF (3824KB) ( 120 )   Save BACKGROUND: Autophagy, as a key regulatory mechanism of cell development, plays an important role in different stages of embryonic development. The mechanism of how autophagy regulates embryonic development through histone modifications is currently unclear.  OBJECTIVE: To investigate the effect of autophagy on trimethylation of lysine 4 on histone H3 (H3K4me3) modification in embryos and its effect on embryonic development.  METHODS: Mouse fertilized eggs were divided into control and autophagy inhibitor-treated groups (chloroquine phosphate-treated group and 3-methyladenine-treated group), and cultured in vitro to different periods of time, and were then classified as early 2-cell embryos, middle 2-cell embryos, late 2-cell embryos, 4-cell embryos, 8-cell embryos, morula stage, and blastocyst stage. Levels of reactive oxygen species, autophagy marker proteins LC3B and P62, DNA loss marker γH2AX, and H3K4me3 were analyzed by immunofluorescence assay in late 2-cell embryos of each group. Changes in H3K4me3 modification in late 2-cell embryos of each group were detected by CUT&Tag.  RESULTS AND CONCLUSION: (1) Autophagy inhibition caused embryo development arrest. (2) There was no significant difference in reactive oxygen species and γH2AX between the autophagy inhibitor-treated groups and control group. (3) H3K4me3 levels were significantly elevated in the autophagy inhibitor-treated group compared with the control group. (4) CUT&Tag results showed a significantly increased H3K4me3 peaks on the proximal promoter region of the genes after autophagy inhibition and an increase of H3K4me3-specific modification genes. These findings suggest that autophagy may affect embryonic development by regulating the level of H3K4me3 modification.  Figures and Tables | References | Related Articles | Metrics

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Spatiotemporal expression of bone morphologic protein 7 in mouse kidney development Sun Yajie, Zhao Xinchen, Bo Shuangling 2026, 30 (5):  1156-1161.  doi: 10.12307/2026.036 Abstract ( 35 )   PDF (1400KB) ( 31 )   Save BACKGROUND: Bone morphogenetic protein 7 is mainly synthesized in the kidney and is expressed at different stages of kidney development, but the spatiotemporal distribution of its expression and its relationship with kidney development have not been systematically reported. OBJECTIVE: To observe the expression of bone morphogenetic protein 7 in mice kidneys during different developmental stages and to explore its potential relationship with kidney development.  METHODS: Immunohistochemical techniques combined with stereological methods and western blot analysis were used to observe and analyze the expression of bone morphogenetic protein 7 in mouse kidney tissues at embryonic days (E)12, 14, 16, 18, and neonatal days (N)1, 3, 7, 14, 24, 40, and 70. RESULTS AND CONCLUSION: (1) The results of immunohistochemistry showed that bone morphogenetic protein 7 was mainly expressed in the nephrogenic zone and immature renal corpuscles during the early stage of kidney development. Subsequently, it was located in mature renal corpuscles and the surrounding distal convoluted tubules, and the expression range gradually increased. After N40 days, bone morphogenetic protein 7 positively expressed in the renal interstitium. (2) Stereology and western blot results showed that the expression level of bone morphogenetic protein 7 gradually decreased with the development of the kidney, reached the lowest level at N7 days, and then slowly increased. To conclude, during the process of kidney development, the expression of bone morphogenetic protein 7 has significant spatiotemporal specificity, and it is hypothesized that it may be related to the development and maturation of renal corpuscles and distal convoluted tubules. Figures and Tables | References | Related Articles | Metrics

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Therapeutic efficacy of extracorporeal shock wave therapy in the upper trapezius muscle area combined with exercise control training in patients with chronic non-specific neck pain Li Haojing, Wang Xin, Song Chenglin, Zhang Shengnan, Chen Yunxin 2026, 30 (5):  1162-1170.  doi: 10.12307/2026.034 Abstract ( 46 )   PDF (1261KB) ( 13 )   Save BACKGROUND: The incidence rate of chronic non-specific neck pain is high and the etiology is unknown. Myofascial pain and deep cervical flexor atrophy are the key factors. Extracorporeal shockwave therapy can improve microcirculation, relieve local pain, and delay the degenerative development of the cervical spine, while motion control training can significantly improve neck muscle strength and endurance and reduce neck pain. However, both methods have limited effectiveness when applied individually. OBJECTIVE: To explore the therapeutic efficacy of extracorporeal shock wave intervention combined with motion control training at the upper trapezius muscle on chronic non-specific neck pain.  METHODS: Forty-two patients with chronic non-specific neck pain recruited from Shenyang Sport University were randomly divided into three groups: a shock wave group (n=14), in which extracorporeal shockwave intervention at the upper trapezius muscle was given for 10-15 minutes, once a week for 4 weeks; a training group (n=14), in which motion control training was given for 40-50 minutes, three times a week for 4 weeks; and a combination group (n=14), in which extracorporeal shockwave intervention at the upper trapezius muscle combined with motion control training was performed for 4 weeks. Patients were assessed for pain intensity, cervical spine function, upper trapezius muscle thickness, hemodynamic parameters, and serum interleukin 6 and tumor necrosis factor α levels before intervention, 1 week and 4 weeks after intervention.  RESULTS AND CONCLUSION: (1) Compared with the pre-intervention period, the visual analogue scale scores and neck disability index in the three groups were lower after 1 and 4 weeks of intervention (P < 0.05), and the visual analogue scale scores and neck disability index in the combination group were lower than those of the shock wave group and the training group (P < 0.05). (2) Compared with the pre-intervention period, the upper trapezius thickness increased in the training group and the combination group after 4 weeks of intervention (P < 0.05); the upper trapezius thickness was greater in the combination group than in the shock wave group and the training group after 4 weeks of intervention (P < 0.05). (3) The shock wave group and the combination group had an increase in the peak systolic velocity of the ascending segment of the transverse carotid artery (P < 0.05) and a decrease in the resistance index (P < 0.05) after 1 and 4 weeks of intervention, while the training group showed an increase in the peak systolic velocity of the ascending segment of the transverse carotid artery  (P < 0.05) and a decrease in the resistance index (P < 0.05) after 4 weeks of intervention. The peak systolic velocity of the ascending segment of the transverse carotid artery in the combination group was higher (P < 0.05) and the resistance index was lower (P < 0.05) than those in the shockwave group and the training group after 1 and 4 weeks of intervention. (4) Compared with the pre-intervention period, the levels of interleukin 6 and tumor necrosis factor α were reduced in the shock wave and combination groups after 1 and 4 weeks of intervention (P < 0.05), and in the training group after 4 weeks of intervention (P < 0.05). After 1 and 4 weeks of intervention, the levels of interleukin 6 and tumor necrosis factor α were lower in the combination group than in the shock wave group and the training group (P < 0.05). To conclude, extracorporeal shock wave combined with motion control training for chronic non-specific neck pain significantly reduces pain and improves neck function, and the mechanism of action may be to promote the blood flow velocity at the trigger point, reduce blood flow resistance, reduce the serum levels of interleukin 6 and tumor necrosis factor α, and increase the thickness of the upper trapezius muscle. Figures and Tables | References | Related Articles | Metrics

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Mechanisms by which aerobic and resistance exercises improve obesity-related cognitive impairment Liu Yu, Lei Senlin, Zhou Jintao, Liu Hui, Li Xianhui 2026, 30 (5):  1171-1183.  doi: 10.12307/2026.023 Abstract ( 39 )   PDF (3034KB) ( 20 )   Save BACKGROUND: Obesity is not only related to metabolic diseases such as diabetes and cardiovascular disease, but also closely related to the increased risk of cognitive decline, dementia and other neurodegenerative diseases. Studies have found that aerobic exercise and resistance exercise can help improve obesity-related cognitive impairment, but their therapeutic effects and related mechanisms of action are still unclear. OBJECTIVE: To explore the protective effects of aerobic and resistance exercises on the nervous center of obesity-related cognitive impairment mice. METHODS: Forty-eight 8-week-old C57BL/6J wild-type male mice were randomly divided into four groups: a control group was fed normally for 20 weeks; a high fat group was fed with high fat diet (60% fat energy) for 20 weeks; an aerobic exercise group was fed with 12 weeks of high-fat diet followed by 8 weeks of aerobic exercise; and a resistance exercise group was fed with 12 weeks of high-fat diet followed by 8 weeks of resistance exercise. After the exercise intervention, body mass was weighed, insulin tolerance and glucose tolerance were tested to evaluate insulin resistance, and cognitive function of mice in each group was detected by new object recognition experiment and Y-maze experiment. The morphology of hippocampal and cortical tissue cells was observed by hematoxylin-eosin staining. The mRNA relative expression levels of tumor necrosis factor-α and interleukin-6 were detected by real-time fluorescence quantitative PCR, and the protein expressions of Bax , Bcl-2, nuclear factor-κB, Cleaved Caspase-1, Caspase-3, synapsin 1 and brain-derived neurotrophic factor were detected by western blot. RESULTS AND CONCLUSION: (1) Compared with the control group, the body mass of mice increased in the high-fat group (P < 0.05), accompanied by insulin resistance and cognitive dysfunction, the expression levels of nuclear factor-κB, Bax, Caspase-3, Cleaved Caspase-1 in the hippocampus were significantly increased (P < 0.05), the expression levels of brain-derived neurotrophic factor, synapsin 1 and Bcl-2 proteins were significantly decreased (P < 0.05), Bcl-2/Bax ratio was significantly decreased (P < 0.05), and the mRNA levels of inflammatory cytokines, tumor necrosis factor-α and interleukin-6, were significantly up-regulated (P < 0.05). (2) Compared with the high-fat group, the above indexes were significantly improved in the aerobic exercise group (P < 0.05), while in the resistance exercise group, the body mass of mice was significantly decreased, the levels of inflammatory cytokines tumor necrosis factor-α and interleukin-6 mRNA were significantly decreased (P < 0.05), the protein expression of Caspase-3 was significantly decreased (P < 0.05), and the protein expression of brain-derived neurotrophic factor was significantly up-regulated (P < 0.05), but no significant changes were observed in the other indexes (P > 0.05). In conclusion, long-term exercise can reduce insulin resistance, down-regulate the expression of nuclear factor-κB pathway, weaken inflammatory response, inhibit neuronal apoptosis and improve synaptic plasticity, resulting in neuroprotective effects, and effectively alleviate obesity-related cognitive dysfunction in obese mice. The therapeutic effect of aerobic exercise is superior to that of resistance exercise. Figures and Tables | References | Related Articles | Metrics

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Acute effects of blood flow restriction in low-intensity resistance training on endothelial function-related inflammatory factors Tao Yunfei, Peng Li 2026, 30 (5):  1184-1195.  doi: 10.12307/2026.020 Abstract ( 30 )   PDF (1081KB) ( 11 )   Save BACKGROUND: Long-term blood flow restriction combined with low-intensity resistance training has been shown to effectively treat obesity by alleviating chronic inflammation and endothelial dysfunction. However, the immediate effects of a single session on serum concentrations of vascular endothelial function and inflammatory biomarkers remain unclear. OBJECTIVE: To explore the short-term effects and recovery capacity of blood flow restriction during low-intensity resistance training on serum biomarkers of vascular endothelial function and inflammation in obese male college students. METHODS: Twenty obese male college students (body mass index > 30 kg/m2, body fat percentage > 25%) were randomly assigned to a control group (0% arterial occlusion pressure) or a blood flow restriction group (80% arterial occlusion pressure). Both groups performed a single session of low-intensity resistance training at an intensity corresponding to a perceived exertion of 11-13 on the Rate of Perceived Exertion Scale. The training was repeated three times, with each session lasting 30 minutes, totaling 1.5 hours. Serum biomarkers were measured before exercise, immediately post-exercise, 1 hour post-exercise, and 24 hours post-exercise. The assessed biomarkers included vascular endothelial function markers, inflammatory markers, and insulin function indicators. RESULTS AND CONCLUSION: (1) Vascular endothelial function: Acute exercise increased vascular endothelial growth factor A concentrations in both groups. The blood flow restriction group significantly elevated serum platelet-derived growth factor and nitric oxide levels (P < 0.05), while the control group showed a significant increase in nitric oxide synthase levels (P < 0.05). Angiotensin II concentrations decreased immediately after acute exercise in both groups but remained significantly higher than baseline in the blood flow restriction group after 24 hours of recovery, and there was a significant difference between the two groups (P < 0.05). (2) Regarding inflammatory markers, the blood flow restriction group induced higher levels of hypoxia and significantly upregulated tumor necrosis factor-α and hypoxia-inducible factor-1α concentrations (P < 0.05). Adiponectin and leptin levels upregulated in both groups, with a more pronounced rise in adiponectin level in the blood flow restriction group than the control group (P < 0.05). Interleukin-6 concentrations decreased in both groups, with a greater reduction in the blood flow restriction group. (3) For insulin function, the blood flow restriction and control groups showed immediate increases and decreases in insulin levels after exercise, respectively, but these returned to below and above baseline levels after 24 hours of recovery. Both groups reduced insulin resistance index in adipose tissue, with a more significant improvement in the blood flow restriction group (P < 0.05). To conclude, compared with low-intensity resistance training, short-term blood flow restriction induces more favorable changes in inflammatory and vascular endothelial biomarkers, improving inflammation and endothelial dysfunction with longer-lasting effects. However, further studies are needed to validate these findings over long-term interventions. Figures and Tables | References | Related Articles | Metrics

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The position and role of 5-hydroxytryptamine in the repair of tissue injury Yu Huifen, Mo Licun, Cheng Leping 2026, 30 (5):  1196-1206.  doi: 10.12307/2026.002 Abstract ( 52 )   PDF (1320KB) ( 17 )   Save BACKGROUND: The 5-hydroxytryptamine system is one of the earliest-developing systems in mammals, playing crucial roles in diverse physiological processes throughout the entire life cycle. Traditionally, research on 5-hydroxytryptamine has primarily focused on its regulatory roles in physiological processes and central nervous system-related diseases. However, recent studies have also highlighted the significant roles of the 5-hydroxytryptamine system in the regenerative medicine.  OBJECTIVE: To review the reparative functions of the central 5-hydroxytryptamine system in brain injury, spinal cord injury, and bone remodeling, as well as the roles of the peripheral 5-HT system in the regeneration and repair of tissues such as the liver, pancreas, intestines, and skin, thereby offering new insights into the development of therapeutic strategies in stem cell therapy, tissue engineering, and regenerative medicine. METHODS: A comprehensive literature search was conducted using the databases “PubMed” and “Google Scholar.” The search terms included: “5-HT,” “regeneration,” “tissue repair,” “5-HT and tissue repair,” “brain injury,” “spinal cord injury,” “bone reconstruction,” “liver regeneration,” “enteric nerve regeneration,” “tissue fibrosis,” “pancreatic regeneration,” “skin repair,” and “inflammation.” Based on the inclusion and exclusion criteria, 118 articles and books were finally included for review and analysis. RESULTS AND CONCLUSION: (1) The central 5-hydroxytryptamine system facilitates cellular regeneration in injuries such as brain damage, spinal cord injury, and bone remodeling, thereby promoting tissue repair following injuries. (2) The peripheral 5-hydroxytryptamine system plays a positive role in the repair of tissues such as the liver, pancreas, intestines, and skin. (3) However, the 5-hydroxytryptamine system also exhibits adverse effects in tissue repair and regeneration, such as promoting tissue fibrosis and exacerbating inflammation. Therefore, it should be used with caution. Figures and Tables | References | Related Articles | Metrics

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Advance in the mechanisms underlying miRNAs in steroid-induced osteonecrosis of the femoral head Wang Zhengye, Liu Wanlin, Zhao Zhenqun 2026, 30 (5):  1207-1214.  doi: 10.12307/2026.003 Abstract ( 43 )   PDF (919KB) ( 15 )   Save BACKGROUND: The pathogenesis of steroid-induced osteonecrosis of the femoral head is complex, involving vascular endothelial injury, osteocyte apoptosis, inflammatory responses, and bone metabolism disorders. MicroRNAs (miRNAs), as key regulators of gene expression, play an important role in steroid-induced osteonecrosis of the femoral head. OBJECTIVE: To comprehensively analyze the regulatory role of miRNAs in steroid-induced osteonecrosis of the femoral head and to evaluate their potential as biomarkers and therapeutic tools.  METHODS: Relevant literature was retrieved from PubMed, Web of Science, CNKI, and WanFang databases using specific keywords, and articles were selected based on the inclusion and exclusion criteria. By reading titles, abstracts, or full texts, articles with poor relevance or repetitive content were excluded, and 76 articles were finally included for analysis. RESULTS AND CONCLUSION: miRNAs regulate gene expression by binding to the 3' untranslated region of target mRNAs, affecting cell differentiation, proliferation, apoptosis, and stress responses. Specific miRNAs such as miR-33-5p, miR-99a, miR-106b-5p, miR-155, miR-146a, and miR-21 play a central regulatory role in vascular injury, inflammatory responses, osteocyte differentiation, and apoptosis in steroid-induced osteonecrosis of the femoral head. Additionally, the expression patterns of miRNAs are closely related to the pathogenesis of steroid-induced osteonecrosis of the femoral head, showing potential as biomarkers. Although miRNAs shows great potential as biomarkers in therapeutic strategies, the current limitation of sample size and lack of multi-population validation restrict the universality and reliability of the results. Moreover, the efficacy and safety of miRNA therapeutic strategies (including off-target effects and delivery issues) remain major challenges in realizing clinical applications. Figures and Tables | References | Related Articles | Metrics

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Intra-articular injections for the treatment of osteoarthritis of the temporomandibular joint: different drugs with multiple combined treatment options Bu Yangyang, Ning Xinli, Zhao Chen 2026, 30 (5):  1215-1224.  doi: 10.12307/2026.005 Abstract ( 55 )   PDF (1054KB) ( 31 )   Save BACKGROUND:  Intra-articular injection therapy is a relatively safe and effective treatment that can effectively relieve clinical signs and symptoms of patients with osteoarthritis of the temporomandibular joint. OBJECTIVE: To summarize new developments in the types of intra-articular injectable drugs and multiple combined treatment options for patients with osteoarthritis of the temporomandibular joint. METHODS: We searched relevant articles included in CNKI and PubMed databases with the keywords of “temporomandibular joint osteoarthritis, steroid hormone, nonsteroidal anti-inflammatory drugs, hyaluronic acid, ozone, chitosan, platelet-rich plasma, stem cell, exosome, intra-articular injection, arthrocentesis, drug therapy, therapy” in Chinese and English, respectively. A total of 67 articles were finally included for review. RESULTS AND CONCLUSION: (1) The application of intra-articular injection therapy in osteoarthritis of the temporomandibular joint is promising. There is a wide range of injectable drugs, including glucocorticoids, hyaluronic acid, chitosan, and platelet-rich plasma. Although the results of the existing studies show good efficacy, large-scale randomized controlled trials are still needed to further verify its safety and efficacy. (2) Different combinations of drugs injected into the joint cavity have shown better efficacy in osteoarthritis of the temporomandibular joint, and future studies should focus on the optimal combinations of different drugs as well as combinations of drugs with other therapeutic options, to provide a more effective treatment option for patients with osteoarthritis of the temporomandibular joint. Figures and Tables | References | Related Articles | Metrics

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Exercise improves microvascular function in patients with type 2 diabetes Wen Fan, Xiang Yang, Zhu Huan, Tuo Yanfang, Li Feng 2026, 30 (5):  1225-1235.  doi: 10.12307/2026.006 Abstract ( 43 )   PDF (1276KB) ( 11 )   Save BACKGROUND: Exercise is an effective way to improve microvascular function in patients with type 2 diabetes. In recent years, exercise has been used as an intervention therapy for microvascular dysfunction in patients with type 2 diabetes. However, few studies have systematically explored the influence of factors, such as "exercise type, exercise intensity and amount of exercise," on microvascular function in patients. To some extent, this limits the formulation of precise exercise prescriptions to improve microvascular dysfunction in patients with type 2 diabetes and the comparison of study results. OBJECTIVE: To investigate the effects of exercise type, intensity, frequency and amount of exercise on microvascular function in patients with type 2 diabetes mellitus, and to make suggestions on exercise prescription. METHODS: The first author used computer to search the studies on the improvement of microvascular function in type 2 diabetes patients involving exercise in CNKI, WanFang, PubMed and other databases. The search terms were “diabetes mellitus, type 2 diabetes mellitus, microcirculation, microvascular reactivity, microvessels, capillaries, vasodilation, blood perfusion volume, endothelial cells, shear stress, exercise, aerobic exercise, resistance exercise, high-intensity exercise” in Chinese and English. The articles were screened by a quick glance at the article titles and abstracts to exclude those that were not closely related to the topic, and finally 60 articles were included for review. RESULTS AND CONCLUSION: (1) Exercise is an effective way to improve microvascular function in patients with type 2 diabetes. Aerobic exercise lasting 12-24 weeks, 3-5 times/week, exercise time > 30 minutes and intensity between 40% and 59% reserve oxygen intake can significantly improve microvascular function in patients with type 2 diabetes. On the basis of aerobic exercise, systemic resistance exercise 2-3 times a week (50%-85% 1RM, every other day) or pressure resistance exercise can obtain better intervention effects. (2) In addition, exercise can improve microvascular function in patients with type 2 diabetes in a “dose-effect” manner, and patients can get better results from the intervention by increasing the amount of exercise, while maintaining safety. (3) The mechanism of exercise improving microvascular function in patients with type 2 diabetes is mainly related to promoting the release of nitric oxide and vascular endothelial growth factor from endothelial cells and inhibiting the release of endothelin1. Figures and Tables | References | Related Articles | Metrics

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Schwann cells promote peripheral nerve regeneration: retrospect and prospect Fu Zhenyi, Li Junhao, Zhang Yating, He Yunkai, Liu Junyu, Wei Yunhao, Liu Jiaxin 2026, 30 (5):  1236-1246.  doi: 10.12307/2026.008 Abstract ( 64 )   PDF (2328KB) ( 47 )   Save BACKGROUND: Peripheral nerve axon rupture seriously affects patients' physical function and mental health. Microsurgery, nerve autograft, nerve allograft, fibrin glue and catheter technology are the main treatments for peripheral nerve injury, each of which has its own advantages and disadvantages, but the overall treatment effect is not satisfactory. Despite the clinical success of Schwann cells in promoting axonal regeneration, there are still many challenges in the treatment with Schwann cells, such as slow expansion of Schwann cells, immune rejection, and low survival rate of transplanted cells. OBJECTIVE: To summarize the role and mechanism of Schwann cells in promoting the regeneration of peripheral nerve axons, and the difficulties and challenges of Schwann cells in the process of nerve regeneration treatment. METHODS: PubMed, Medline, WanFang, VIP, and CNKI were searched by computer using the search terms of “Schwann cells, synaptic Schwann cell, macrophage, peripheral nerve axon rupture, Wallerian degeneration, Peripheral nerve axon regeneration, Central nervous system repair” in English and Chinese. Literature related to Schwann cell proliferation and differentiation, promotion of peripheral nerve regeneration, and clinical applications was retrieved from database inception to October 2024, and a total of 95 articles were finally included for review. RESULTS AND CONCLUSION: Schwann cells interact with macrophages, T cells and other cells, to initiate the regeneration process through signaling pathways, including Krox20/C-Jun, NRG-1/ErbB, Notch, MAPK, and PI3K/Akt/mTOR, synthesize and release nerve growth factors, and thus promote regeneration of the peripheral nervous system. Schwann cells have been experimentally demonstrated to have great potential in peripheral nerve repair and are expected to become the key target of therapeutic intervention. However, there are still problems such as difficulties in cell harvest and culture, as well as the occurrence of other diseases during the treatment process. Figures and Tables | References | Related Articles | Metrics

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Regeneration and repair of oral alveolar bone defects Liu Xinyue, Li Chunnian, Li Yizhuo, Xu Shifang 2026, 30 (5):  1247-1259.  doi: 10.12307/2026.011 Abstract ( 64 )   PDF (1654KB) ( 23 )   Save BACKGROUND: Developing a material that promotes alveolar bone regeneration and has good properties is of great significance for the treatment of alveolar bone defects. OBJECTIVE: To summarize the research on alveolar bone defect regeneration and repair in the past 5 years, classify and introduce new materials and drugs, so as to grasp the latest progress in related fields. METHODS: “Alveolar bone, alveolar bone defect, alveolar bone regeneration, mechanism, biomaterials, nanoscaffolds, hydrogels, medications, anti-inflammatory drugs, simvastatin, metformin, traditional Chinese medicine, growth factor, stem cell” were used as search terms in Chinese and English for literature retrieval in CNKI and PubMed, respectively. A total of 117 articles were finally obtained for review and analysis. RESULTS AND CONCLUSION: The application of biomaterials provides a scaffold structure for alveolar bone regeneration and can also be used as a bone substitute to repair bone defects. Topical and systemic applications of Western and Chinese medicines can control inflammation and promote bone regeneration. Materials loaded with various growth factors have the effect of osteogenesis and can promote the repair of alveolar bone defects. In stem cell tissue engineering, the seed cells are osteogenic and fibrogenic, which can differentiate into osteoblasts to generate new bone. In recent years, research has been keen on the combination of the above to develop new, biocompatible, and slow-release drugs or materials to promote the regeneration and repair of alveolar bone defects.  Figures and Tables | References | Related Articles | Metrics

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Safety and efficacy of immunoadsorption therapy for rheumatoid arthritis: a network meta-analysis and systematic review Zheng Yin, Wu Zhenhua, Zhang Cheng, Ruan Kexin, Gang Xiaolin, Ji Hong 2026, 30 (5):  1260-1268.  doi: 10.12307/2026.053 Abstract ( 42 )   PDF (1386KB) ( 12 )   Save OBJECTIVE:  To evaluate the efficacy and safety of different immunosorbent columns in the treatment of rheumatoid arthritis through a network meta-analysis, and provide evidence-based basis for clinical diagnosis and treatment. METHODS: By computer, the databases of VIP, WanFang, CNKI, PubMed, CBM, CochraneLibrary, and Web of Science were searched for published cohort studies of immunosorbent column for the treatment of rheumatoid arthritis, with a time limit until August 2024. The quality of the included randomized controlled trials was assessed using the Cochrane5.4 manual. The quality of retrospective cohort studies were evaluated via the Newcastle-Ottawa Scale (NOS). Bayesian network meta-analysis was performed using R4.1.1 software. RESULTS: A total of 13 studies were included, with a total sample size of 891 cases, and 4 immunosorbent columns were included. The results of the network meta-analysis showed that the top three orders that reduce C-reactive protein level: HA280 adsorption column + conventional Western medicine > PH-350 adsorption column + conventional Western medicine > A protein adsorption column; the top three orders that reduce erythrocyte sedimentation rates: leukocyte adsorption column > HA280 adsorption column + conventional Western medicine > PH-350 adsorption column + conventional western medicine; the top three orders that reduce swollen joint count: leukocyte adsorption column > A protein adsorption column + conventional western medicine > PH-350 type adsorption column + conventional Western medicine; the top three orders that reduce tenderness joint counts: leukocyte adsorption column > A protein adsorption column + conventional western medicine > PH-350 adsorption column + conventional Western medicine; the top three orders that reduce patients' disease activity evaluation: PH-350 adsorption column + conventional western medicine > leukocyte adsorption column > A protein adsorption column; the top three orders that reduce visual analogue scale scores: PH-350 adsorption column + conventional Western medicine > A protein adsorption column > leukocyte adsorption column; the top three orders that reduce physician’s disease activity assessment: PH-350 adsorption column + conventional Western medicine > leukocyte adsorption column > conventional Western medicine. CONCLUSION: Based on the 13 articles, in terms of reducing C-reactive protein level, HA280 adsorption column and conventional Western medicine are the preferred choice. In terms of reducing erythrocyte sedimentation rate, swollen joint count, and tender joint count, leukocyte adsorption column is the preferred choice. In terms of reducing patient’s disease activity evaluation, physician’s disease activity evaluation and visual analogue scale scores, PH-350 adsorption column and conventional Western medicine are the first choice. Different immunosorbent columns can be reasonably and accurately selected according to the patient’s specific conditions. Figures and Tables | References | Related Articles | Metrics

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Physical exercise improves physical function in burn patients: a systematic review and meta-analysis Chen Qiang, Wu Wenjuan, Jiang Shuhua, Huang Da 2026, 30 (5):  1269-1281.  doi: 10.12307/2026.016 Abstract ( 51 )   PDF (4960KB) ( 26 )   Save OBJECTIVE: Some studies have shown that physical exercise can effectively improve knee extensor strength and cardiorespiratory function in burn patients; some studies have also shown that physical exercise is not effective in improving respiratory function in burn patients. Improvement effects of physical exercise on physical functions (muscle function, walking function, cardiopulmonary function, and lean body mass) of burn patients were evaluated by a systematic evaluation and meta-analysis. METHODS: Based on databases including Web of Science, PubMed, Embase, Cochrane Library, CNKI, WanFang, and the Chinese Biomedical Database, literature on the improvement of physical function in burn patients through physical exercise was searched using subject headings and free terms. With muscle function, walking ability, cardiopulmonary function, and lean body mass as the primary outcome measures, a meta-analysis was conducted to compare the efficacy of physical exercise with traditional physical therapy or conventional care methods. RESULTS: A total of 38 papers were included, of which 26 papers were included in the meta-analysis, involving 1 658 patients. Meta-analysis results showed that: (1) Physical exercise significantly enhances the knee extensor strength of the dominant leg in burn patients (mean difference [MD]=8.34, 95% confidence interval [CI]: 6.95-9.72, P < 0.000 01), increases quadriceps strength, peak oxygen uptake, forced vital capacity and maximum ventilation volume in 1 second, and resting heart rate (standardized mean difference [SMD]=4.41, 95% CI: 2.52-6.30, P < 0.000 01; MD=4.91, 95% CI: 3.52-6.29, P < 0.000 01; MD=5.86, 95% CI: 0.09-11.63, P=0.05; MD=6.90, 95% CI: 2.93-10.87, P=0.000 7; MD=5.03, 95% CI: 1.45-8.61, P=0.006), and improves the 6-minute walking distance, gait parameters, and total lean body mass (MD=45.29, 95% CI: 24.7-65.89, P < 0.0001; SMD=7.84, 95% CI: 6.05-9.63, P < 0.000 01; MD=2.47, 95% CI: 2.01-2.93, P < 0.000 01). (2) The subgroup analysis results indicated that the improvement in knee extensor strength of the dominant leg may be better in children than in adults and better in the extra-heavy group than in the heavy group. Improvement in the 6-minute walking distance is better in children than in adults, and higher degree of burn indicates better improvement effects, with no difference from the control group for < 12 weeks. Peak oxygen uptake may be better in adults and severe burn groups than in children and moderate burn groups, resistance combined with aerobic exercise modalities may be better than aerobic exercise alone, and exercise duration > 60 minutes may be better than < 60 minutes. CONCLUSION: Physical activity is effective in improving physical function in burn patients, as evidenced by improvements in muscle strength, walking ability, cardiorespiratory fitness, and lean body mass. The quality of evidence recommended for all indicator results is moderate or below, with imprecision and inconsistency being the main factors for downgrading. Therefore, more high-quality randomized controlled trials are needed in the future to verify the reliability of the results. Figures and Tables | References | Related Articles | Metrics

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Effects of different neuromodulatory stimulation modalities on non-motor symptoms in Parkinson’s patients: a network meta-analysis Leng Xiaoxuan, Zhao Yuxin, Liu Xihua 2026, 30 (5):  1282-1293.  doi: 10.12307/2026.032 Abstract ( 38 )   PDF (1874KB) ( 9 )   Save OBJECTIVE: It has been confirmed that neuromodulation technology can improve the clinical symptoms of patients with Parkinson’s disease, and there are differences in the efficacy of different neuromodulation stimulation methods. Herein, a network meta-analysis was used to evaluate the efficacy of different neuromodulation stimulation modalities in improving non-motor symptoms such as sleep disorders and depression and anxiety in patients with Parkinson’s disease, thereby exploring the optimal neuromodulation stimulation regimen. METHODS: The Chinese Biomedical Literature Database, WanFang Database, VIP Database, CNKI Database, Web of Science, PubMed, The Cochrane Library, and EMbase databases were searched for randomized controlled trials on neuromodulation techniques to improve sleep disorders, depression and anxiety in patients with Parkinson’s disease. The control group was treated with conventional treatments (drugs, conventional rehabilitation therapy, etc.) or sham stimulation, and the experimental group was supplemented with neuromodulation technology on the basis of the control group. The quality of the included studies was evaluated using the PEDro scale and the deviation risk assessment tool recommended by the Cochrane Collaboration. RevMan 5.4 and Stata 17.0 were used for network meta-analysis of the four outcomes (sleep disorders, anxiety symptoms, depressive symptoms, and quality of life). RESULTS: (1) Twenty-nine randomized controlled trials involving six neuromodulation stimulation modalities were included. These modalities were transcranial direct current stimulation, high-frequency repetitive transcranial magnetic stimulation, low-frequency repetitive transcranial magnetic stimulation, deep brain stimulation of the subthalamic nucleus, deep brain stimulation of the globus pallidus, multi-target deep brain stimulation. (2) The results of network meta-analysis showed that compared with conventional treatment, transcranial direct current stimulation [standardized mean difference (SMD)=-2.57, 95% confidence interval (CI)=-4.52 to -0.63, P < 0.05) had the best effect in improving sleep disorders in patients with Parkinson’s disease. In terms of improving depressive symptoms, deep brain stimulation of the globus pallidus (SMD=-1.00, 95% CI=-1.87 to -0.14, P < 0.05) had the best effect, followed by low-frequency repetitive transcranial magnetic stimulation (SMD=-0.91, 95%CI=-1.60 to -0.23, P < 0.05), deep brain stimulation of the subthalamic nucleus (SMD=-0.82, 95% CI=-1.56 to -0.08, P < 0.05), and high-frequency repetitive transcranial magnetic stimulation (SMD=-0.75, 95% CI=-0.97 to -0.53, P < 0.05). In terms of improving anxiety symptoms, high-frequency repetitive transcranial magnetic stimulation (SMD=-0.86, 95% CI=-1.54 to -0.18, P < 0.05) had the best effect. In terms of improving the quality of life, deep brain stimulation of the globus pallidus (SMD=-0.79, 95% CI=-1.55 to -0.04, P < 0.05) had the best efficacy, followed by high-frequency repetitive transcranial magnetic stimulation (SMD=-0.63, 95% CI=-0.90 to -0.36, P < 0.05) and transcranial direct current stimulation (SMD=-0.50, 95% CI=-0.80 to -0.19, P < 0.05).  CONCLUSION: Neuromodulation technology has significant efficacy in improving non-motor symptoms in patients with Parkinson’s disease. Transcranial direct current stimulation has the best efficacy in improving sleep disorders, deep electrical stimulation of the medial cerebral part of the globus pallidus has the best efficacy in improving depressive symptoms, high-frequency repetitive transcranial magnetic stimulation has the best efficacy in improving anxiety symptoms, and deep electrical stimulation of the globus pallidus has the best efficacy in improving quality of life. Figures and Tables | References | Related Articles | Metrics

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Effects of inflammation on serum hepcidin and iron metabolism related parameters in patients with type 2 diabetes mellitus: a meta-analysis Wen Xiaolong, Weng Xiquan, Feng Yao, Cao Wenyan, Liu Yuqian, Wang Haitao 2026, 30 (5):  1294-1301.  doi: 10.12307/2026.043 Abstract ( 41 )   PDF (1613KB) ( 9 )   Save OBJECTIVE: Disorders in iron metabolism increase the risk of type 2 diabetes mellitus. Hepcidin play an important role in maintaining iron homeostasis in the body, but its level increases with increased inflammation. Changes in hepcidin and iron homeostasis and the extent of their association with inflammation in people with and without type 2 diabetes mellitus are unknown. Meta-analysis was used to evaluate the effect of inflammation on serum hepcidin and iron metabolism related parameters in patients with type 2 diabetes mellitus. METHODS: CNKI, PubMed, Web of Science and EBSCOhost databases were searched by computer to collect observational studies related to inflammatory index and hepcidin in patients with type 2 diabetes mellitus. The search time was from September 1, 2000 to September 30, 2024. Three researchers independently screened the literature, extracted data and evaluated the quality of the included literature. Meta-analysis was performed by Review Manager 5.3, Stata 17.0 and GraphPad Prism 8.0.2 software. RESULTS: A total of 15 articles (17 studies) involving 3 159 participants, including 1 357 patients with type 2 diabetes mellitus, were included. Meta-analysis results showed that compared with the control group, patients with type 2 diabetes mellitus had higher levels of serum hepcidin [standardized mean difference (SMD)=0.35, 95% confidence interval (CI) (0.05, 0.65), P < 0.05], serum ferritin (SMD=0.49, 95% CI (0.21, 0.78), P < 0.01) and serum transferrin (SMD=0.19, 95% CI (0.00, 0.37), P < 0.05). Subgroup analysis results indicated that inflammation had a significant effect on serum hepcidin (SMD=0.76, 95% CI (0.17, 1.34), P < 0.05) and serum ferritin (SMD=0.77, 95% CI (0.06, 1.47), P < 0.05) in patients with type 2 diabetes mellitus. CONCLUSION: Hepcidin concentration is positively correlated with type 2 diabetes mellitus. Inflammation is one of the risk factors of type 2 diabetes mellitus. Early prevention of inflammation has certain significance in preventing iron metabolism disorder in patients with type 2 diabetes mellitus. Figures and Tables | References | Related Articles | Metrics

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Increased risk of osteoporotic pathological fractures associated with sterol esters: evidence from IEU-GWAS and FinnGen databases Gao Zengjie, , Pu Xiang, Li Lailai, Chai Yihui, Huang Hua, Qin Yu 2026, 30 (5):  1302-1310.  doi: 10.12307/2026.301 Abstract ( 33 )   PDF (2229KB) ( 15 )   Save BACKGROUND: Although previous studies have reported associations between lipids and the risk of osteoporotic pathological fractures, the specific causal relationships between lipid level and osteoporotic pathological fractures remain unclear.  OBJECTIVE: To elucidate the causal relationship between lipids and osteoporotic pathological fractures using a two-sample bidirectional Mendelian randomization analysis. METHODS: The data for 178 lipid metabolites were obtained from the IEU-GWAS database (developed by the MRC Integrative Epidemiology Unit at the University of Bristol, UK, which provides extensive summary data from genome-wide association studies), while osteoporotic pathological fracture data (from 173 619 European participants) were acquired from the FinnGen database (constructed by the Finnish national gene research program, focusing on investigating relationships between genomics and health/disease in the Finnish population). Osteoporotic pathological fracture data were used as the outcome variable, with lipids serving as exposures, for the bidirectional Mendelian randomization study to evaluate the causal effects of different lipids on osteoporotic pathological fractures. The UK Biobank database was employed as a validation set by switching the outcome variable to verify the findings horizontally. RESULTS AND CONCLUSION: (1) The inverse variance weighted analysis indicated that each unit increase in sterol ester (27:1/20:2) levels was associated with a 25.55% increase in the risk of osteoporotic pathological fractures (odds ratio=1.256, 95% confidence interval: 1.001-1.575, P = 0.049), suggesting a significant positive correlation between elevated sterol ester levels and increased fracture risk. Reverse Mendelian randomization analysis revealed a significant negative association between osteoporotic pathological fractures and three types of phosphatidylcholine. Horizontal validation yielded consistent results, confirming sterol ester as a risk factor for osteoporotic pathological fractures. (2) The results indicate that sterol ester is a risk factor for osteoporotic pathological fractures, while phosphatidylcholine serves as a protective factor. These findings strengthen the evidence supporting the effect of lipids on the risk of osteoporotic pathological fractures. Although the GWAS data used in this study were derived from European populations, given the broad commonality of human genetics, the results provide valuable reference significance for improving osteoporosis in Chinese populations through lipid regulation. Figures and Tables | References | Related Articles | Metrics

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Gene-predicted associations between 731 immune cell phenotypes and rheumatoid arthritis Liu Fengzhi, Dong Yuna, Tian Wenyi, Wang Chunlei, Liang Xiaodong, Bao Lin 2026, 30 (5):  1311-1319.  doi: 10.12307/2026.045 Abstract ( 42 )   PDF (4701KB) ( 32 )   Save BACKGROUND: Rheumatoid arthritis is widely prevalent worldwide, with its high incidence and universality that considerably affects patients’ quality of life. Previous studies have focused on a few immune cells or cytokines, whereas this study comprehensively provides a more complete view of the immune mechanisms in rheumatoid arthritis. OBJECTIVE: To explore the causal relationship between 731 immune cell phenotypes and rheumatoid arthritis using the Mendelian randomization method, thereby providing evidence of causality. METHODS: The 731 immune cell phenotypes used in this study were sourced from the GWAScatalog database, jointly developed by the National Human Genome Research Institute (NHGRI) and the European Bioinformatics Institute (EBI). The rheumatoid arthritis data were from the Finngen database, developed by the Finnish Institute for Molecular Medicine (FIMM). The inverse variance weighting method was employed as the primary analytical approach. Additionally, multiple analytical methods, including MR-Egger, weighted mode, simple mode, and weighted median, were concurrently utilized to complement the final results. Sensitivity analyses (Cochran’s Q test, MR-Egger regression, and MR-presso analysis) were also conducted to verify the stability and feasibility of the data. RESULTS AND CONCLUSION: (1) After excluding results through heterogeneity testing, the inverse variance weighting analysis indicated that 10 absolute cell counts, 15 median fluorescence intensities of surface antigen levels, 1 morphological characteristic, and 9 relative cell counts had a causal relationship with the occurrence of rheumatoid arthritis. (2) According to cell classification, this study found that seven types of B cells, seven types of classical dendritic cells, six types of mature T cells, four types of monocytes, three types of myeloid cells, three types of TBNK cells (lymphocyte subset T cells, B cells and natural killer cells), and five types of Tregs had a causal association with the occurrence of rheumatoid arthritis. (3) Through comprehensive bidirectional two-sample MR analysis, we demonstrated the complex causal relationships between multiple immune phenotypes and rheumatoid arthritis, highlighting the intricate interaction patterns between the immune system and rheumatoid arthritis. These results provide new biomarkers for the early screening and diagnosis of rheumatoid arthritis in China, and help to improve the diagnostic accuracy and sensitivity. Figures and Tables | References | Related Articles | Metrics

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A visualized analysis of research hotspots in high-frequency repetitive transcranial magnetic stimulation from the macroscopic perspective Yang Zeyu, Zhi Liang, Wang Jia, Zhang Jingyi, Zhang Qingfang, Wang Yulong, Long Jianjun 2026, 30 (5):  1320-1330.  doi: 10.12307/2026.033 Abstract ( 47 )   PDF (4618KB) ( 26 )   Save BACKGROUND: High-frequency repetitive transcranial magnetic stimulation has garnered significant attention due to its potential non-invasive benefits in modulating brain function. However, no studies have comprehensively analyzed the current research landscape and development trends of this field from a macroscopic perspective. OBJECTIVE: To explore research hotspots, current trends, and emerging frontiers in the field of high-frequency repetitive transcranial magnetic stimulation through visualized analysis. METHODS: Data were collected from the Web of Science Core Collection database from January 1, 2014 to November 15, 2024. CiteSpace was used for analyzing publication volume, collaborations among countries/regions, institutions and authors, citation analysis of journals and co-cited literature, as well as disciplinary distribution. Additionally, keyword co-occurrence, clustering, and burst analyses were conducted, and visualized knowledge maps were generated. RESULTS AND CONCLUSION: A total of 860 articles were included. The publication volume of high-frequency repetitive transcranial magnetic stimulation showed an overall upward trend from 2014 to 2022, followed by a decline from 2022 to 2024. China had the highest publication volume, while Ghent University ranked as the most productive institution. Universities acted as the most high-output institutions. Chris Baeken from Ghent University was identified as the most prolific author. Collaboration among leading authors and institutions worldwide remained limited. The main research hotspots in this field were associated with keywords such as depression, stroke, neuropathic pain, and Parkinson’s disease. Burst keywords focused on mild cognitive impairment, reflecting a diversification in research directions. The overall research activity in high-frequency repetitive transcranial magnetic stimulation continues to rise, with primary focuses on its clinical applications for psychiatric and neurological disorders, as well as explorations of its underlying mechanisms. Future research may focus on optimizing treatment parameters for targeting different brain regions in clinical applications and expanding its applications and mechanisms across various domains. Figures and Tables | References | Related Articles | Metrics

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Relationship between plasma proteins and pulmonary arterial hypertension and potential therapeutic targets Zhang Cuicui, Chen Huanyu, Yu Qiao, Huang Yuxuan, Yao Gengzhen, Zou Xu 2026, 30 (5):  1331-1340.  doi: 10.12307/2026.015 Abstract ( 43 )   PDF (1941KB) ( 11 )   Save BACKGROUND: Pulmonary arterial hypertension is a destructive cardiopulmonary disease for which there is no cure. An association between plasma proteins and pulmonary arterial hypertension has been suggested, but the causal relationship has not been specifically elucidated.  OBJECTIVE: To elucidate the causal relationship between plasma proteome and pulmonary arterial hypertension using a two-sample Mendelian randomization method, thereby searching for potential therapeutic targets for pulmonary arterial hypertension. METHODS: Plasma Protein Gene-Wide Association Analysis Statistics for 4 907 Aptamer Measurements in 35 559 Icelanders from the Icelandic Database; Genome-wide association analysis statistics for pulmonary arterial hypertension were obtained from the Finn Gen database, version R9, including 234 cases and 265 626 controls. Analyses were performed using Mendelian randomization and Bayesian co-localization analysis, the findings were examined using sensitivity analyses, and protein-protein interaction network maps were constructed to explore the causal relationship between plasma proteins and pulmonary arterial hypertension. RESULTS AND CONCLUSION: (1) The results of inverse variance weighting, maximum likelihood and Wald ratio methods showed 19 proteins causally associated with pulmonary arterial hypertension (P < 0.05). Among them, 10 plasma proteins, including Beta-1,3-N-acetylglucosaminyltransferase manic fringe (odds ratio [OR]=0.12, 95% confidence interval [CI] 0.02-0.61, P=0.01) and interferon alpha/beta receptor 1 (OR=0.45, 95% CI 0.24-0.84, P=0.012), might be associated with a reduced risk of pulmonary arterial hypertension. In contrast, nine plasma proteins, such as glucoside xylosyltransferase 1 (OR=3.48, 95% CI 1.51-8.00, P=0.003) and plasminogen (OR=42.78, 95% CI 2.49-734.31, P=0.01), might be associated with an increased risk of pulmonary arterial hypertension. After the false discovery rate was corrected, 19 proteins remained significantly associated with pulmonary arterial hypertension. (2) Multiple sensitivity analyses such as the MR-Egger intercept test and leave-one-out method showed no horizontal multiplicity or heterogeneity in the results of the study, indicating the stability of the study’s results. (3) Bayesian co-localization analysis showed that six plasma proteins, including plasminogen (PPH4=1.0) and glucoside xylosyltransferase 1 (PPH4=0.94), had PPH4 > 0.8, suggesting that plasma proteins and the genome-wide association study of pulmonary arterial hypertension had similar causal variance in terms of genetic association. (4) By constructing a protein-protein interaction network map, plasminogen, Annexin A1, fibrinogen gamma chain and matrix metalloproteinase 7 were found to be core proteins. (5) The article used Mendelian randomization analysis to reveal a potential causal association between 4 907 plasma proteins and pulmonary arterial hypertension, suggesting that plasma proteins may be potential therapeutic targets for pulmonary arterial hypertension. The core proteins identified in the study also provide a theoretical basis for further in-depth study of the pathophysiological mechanisms of pulmonary arterial hypertension. Secondly, analyses using the large-scale international databases of Iceland and FinnGen provide new research directions and treatment ideas for pulmonary arterial hypertension in specific populations and environments, as well as ideas and methods that can be used to prevent and treat pulmonary arterial hypertension in China. Figures and Tables | References | Related Articles | Metrics