Aerobic exercise promotes remodeling of the energy metabolism network in the skeletal muscle of mice with sarcopenic obesity

doi:10.12307/2025.631

Chinese Journal of Tissue Engineering Research ›› 2025, Vol. 29 ›› Issue (17): 3596-3604.doi: 10.12307/2025.631

Previous Articles Next Articles

Aerobic exercise promotes remodeling of the energy metabolism network in the skeletal muscle of mice with sarcopenic obesity

Chen Cong1, 2, 3, Wu Huijuan1, 4, Hu Yue1, 4, Zhou Huanghao1, 4, Huang Chunxiu1, 4

1National-Local Joint Engineering Research Center of Rehabilitation Medicine Technology, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, Fujian Province, China; 2Rehabilitation Industry Institute, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, Fujian Province, China; 3Fujian Key Laboratory of Cognitive Rehabilitation, Fuzhou 350122, Fujian Province, China; 4School of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, Fujian Province, China

Received:2024-05-30 Accepted:2024-07-27 Online:2025-06-18 Published:2024-11-01
Contact: Chen Cong, National-Local Joint Engineering Research Center of Rehabilitation Medicine Technology, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, Fujian Province, China; Rehabilitation Industry Institute, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, Fujian Province, China; Fujian Key Laboratory of Cognitive Rehabilitation, Fuzhou 350122, Fujian Province, China
About author:Chen Cong, PhD, Associate professor, National-Local Joint Engineering Research Center of Rehabilitation Medicine Technology, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, Fujian Province, China; Rehabilitation Industry Institute, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, Fujian Province, China; Fujian Key Laboratory of Cognitive Rehabilitation, Fuzhou 350122, Fujian Province, China Wu Huijuan, Master candidate, National-Local Joint Engineering Research Center of Rehabilitation Medicine Technology, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, Fujian Province, China; School of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, Fujian Province, China Chen Cong and Wu Huijuan contributed equally to this work.
Supported by:
National Natural Science Foundation of China, No. 32271175 (to CC); Fujian Provincial Natural Science Foundation, No. 2021J01960 (to CC)

Abstract

Abstract: BACKGROUND: Sarcopenia obesity is characterized by the coexistence of sarcopenia and obesity with a continuously increasing prevalence. Aerobic exercise can alleviate the progression of sarcopenic obesity, but the overall metabolic changes in skeletal muscle after exercise are still unclear.
OBJECTIVE: To investigate the effects of exercise on various aspects of the energy metabolic pathways in the skeletal muscle of mice with sarcopenic obesity.
METHODS: Male C57BL/6J mice were randomly divided into normal control (normal diet) and model (high-fat diet) groups. After 12 weeks of feeding, sarcopenic obesity model mice were screened by body mass and behavior assessments. The sarcopenia obesity mice were then divided into the sedentary and exercise groups. Mice in the exercise group were subjected to treadmill training on the basis of a high-fat diet. After 8 weeks of intervention, body mass, lipid metabolism, muscle volume of calf muscle group of the hind limb, skeletal muscle morphology, and expressions of energy metabolic pathway-related genes were detected.
RESULTS AND CONCLUSION: Compared with the normal control group, the levels of triglycerides, total cholesterol, and free fatty acid in the sedentary group were significantly increased, along with significantly increased lipid droplets in skeletal muscle (P < 0.05). Compared with the sedentary group, all of the above indicators in the exercise group showed a significant decreasing trend (P < 0.05). Compared with the normal control group, grip strength and fatigue latency time, muscle volume, and fiber cross-sectional area were significantly decreased in the sedentary group, but the mRNA expression of Atrogin-1 and Murf-1
was elevated (P < 0.05). Compared with the sedentary group, grip strength and fatigue latency time, muscle volume, and fiber cross-sectional area were significantly improved in the exercise group (P < 0.05), while the mRNA expression of Atrogin-1 and Murf-1 was reduced (P < 0.05). Compared with the normal control group, the mRNA expression of intramuscular transcription factors Pparα and Pgc-1α was decreased in the sedentary group (P < 0.05), the mRNA expression of fatty acid synthesis-related enzymes Srebp1c and Fasn was elevated (P < 0.05), and the mRNA expression of the β-oxidation system Cpt1β, Acox1, Acox3 and fatty acid metabolism Arf1 and Plin3 was decreased (P < 0.05). Compared with the sedentary group, the abnormal expression of the above genes was significantly reversed in the exercise group (P < 0.05). To conclude, aerobic exercise can alleviate lipid deposition and improve muscle quality and strength of sarcopenic obesity mice by regulating the expression of genes in the intramuscular energy metabolism network.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

Key words: sarcopenic obesity, treadmill exercise, aerobic exercise, lipid metabolism, skeletal muscle, fatty acid β-oxidation, fatty acid metabolism

CLC Number:

Chen Cong, , , Wu Huijuan, , Hu Yue, , Zhou Huanghao, , Huang Chunxiu. Aerobic exercise promotes remodeling of the energy metabolism network in the skeletal muscle of mice with sarcopenic obesity[J]. Chinese Journal of Tissue Engineering Research, 2025, 29(17): 3596-3604.

Figures/Tables 5

2.1 实验动物数量分析 36只C57BL/6J小鼠的数据全部纳入结果分析。 2.2 各组小鼠体质量及行为学变化小鼠在适应性喂养1周后进行分组，正常对照组和造模组初始体质量、抓力以及疲劳转棒停留时间比较均无显著性意义(P > 0.001)。经过12周喂养后，与正常对照组相比，造模组小鼠的体质量增加了20%，见图1A，小鼠血清三酰甘油、总胆固醇、游离脂肪酸水平可见显著性升高(P < 0.001)，见图1B。行为学检测结果显示，造模组小鼠的抓力和疲劳转棒停留时间均显著低于正常对照组(P < 0.001)，以上结果提示高脂饮食诱导的肌少性肥胖小鼠模型建立成功，见图1C，D。 2.3 各组小鼠体质量与脂质水平变化运动干预结束后，与正常对照组相比，静坐组小鼠体质量、血清三酰甘油(P < 0.05)、总胆固醇(P < 0.001)和游离脂肪酸水平(P < 0.001)显著升高；与静坐组相比，运动组小鼠的体质量、血清三酰甘油(P < 0.05)、总胆固醇(P < 0.001)和游离脂肪酸(P < 0.001)水平显著降低。值得注意的是，与正常对照组相比，静坐组小鼠在血清总胆固醇水平表现出89%的显著性升高，运动组小鼠也观察到了总胆固醇水平的增加，仅为54%，而运动组小鼠总胆固醇水平相比于静坐组小鼠表现出23%的相对降低。这一结果揭示了运动干预对调节胆固醇水平具有潜在的积极影响，但是从各组间的差异幅度来看其影响程度可能有限。此外，油红O染色结果显示，与正常对照组相比，静坐组小鼠骨骼肌出现明显的脂肪浸润，运动可显著减少肌少性肥胖小鼠骨骼肌内脂滴沉积现象，见图2。 2.4 各组小鼠后肢小腿肌群体积变化 MRI扫描显示，静坐组相较于正常对照组小鼠后肢小腿肌群的肌肉形态和结构均发生了显著变化，具体表现为肌肉体积显著缩减(P < 0.05)。运动训练干预8周后，运动组相较于静坐组小鼠后肢小腿肌群的肌肉形态和组织结构得以改善，后肢肌肉体积显著增加(P < 0.001)，见图3。 2.5 各组小鼠抓力和疲劳转棒停留时间小鼠抓力测试仪结果显示，静坐组小鼠抓力显著低于正常对照组(P < 0.01)，而运动干预后小鼠抓力显著升高(P < 0.01)。此外，在疲劳转棒测试中，静坐组小鼠的停留时间相较于正常对照组显著缩短(P < 0.001)，运动干预后小鼠的停留时间显著延长(P < 0.01)，见图4。 2.6 各组小鼠骨骼肌肌纤维横截面积变化苏木精-伊红染色表明，静坐组小鼠骨骼肌肌纤维横截面积明显小于正常对照组(P < 0.05)，组织结构呈现不规则，肌纤维间排列较为稀疏，且肌肉纤维内部存在许多空隙。与静坐组相比，运动组小鼠的肌纤维横截面积显著增加(P < 0.01)，肌纤维间的空隙减少，纤维内部的空洞变小，肌细胞构造趋于完整，见图5。 2.7 各组小鼠肌萎缩标志基因表达变化 Atrogin-1和Murf-1是两种E3泛素化连接酶，肌萎缩过程中促进肌细胞蛋白质的分解。RT-qPCR检测结果显示，与正常对照组相比，静坐组小鼠骨骼肌Atrogin-1和Murf-1 mRNA表达水平显著上调(P < 0.05)。与静坐组相比，运动组小鼠骨骼肌Atrogin-1和Murf-1 mRNA表达水平均显著下调(P < 0.01，P < 0.05)，见图6。 2.8 各组小鼠能量代谢相关基因表达变化在正常生理状态下，脂肪酸的吸收、分解和合成呈现动态平衡从而避免了细胞内脂质的堆积。与正常对照组相比，静坐组小鼠骨骼肌中脂肪酸代谢相关的转录因子Pparα和Pgc-1α mRNA表达水平显著下调(P < 0.05)，而运动干预后Pparα和Pgc-1α mRNA表达水平显著上调(P < 0.05)。此外，与正常对照组相比，静坐组小鼠骨骼肌中β脂肪酸氧化通路相关基因Cpt1β(P < 0.01)，Acox1(P < 0.01)和Acox3(P < 0.05) mRNA表达水平均显著下调，而运动干预后Cpt1β、Acox1和Acox3的mRNA表达水平显著上调(P < 0.01)。与正常对照组相比，静坐组小鼠骨骼肌中脂质合成相关基因Srebp1c和Fasn mRNA表达水平显著上调(P < 0.05)，Arf1和Plin3 mRNA表达水平则降低(P < 0.05)。运动干预有效地逆转了这些基因的表达变化(P < 0.05)，见图7。由此可见，运动干预能显著下调骨骼肌内脂肪酸合成关键基因表达，同时上调脂肪酸氧化基因表达，这一双向调节不仅抑制了脂肪酸的合成过程，还加速了其在体内的分解过程，从而优化了能量代谢途径并提高了脂肪的氧化利用率。以上结果表明运动对于调节骨骼肌中脂质代谢平衡具有重要作用。"

References

[1] 刘妍慧,陈树春.2022年欧洲临床营养与代谢学会和欧洲肥胖研究学会《肌肉减少性肥胖的定义和诊断标准共识》解读及启示[J].中国全科医学,2023,26(12):1422-1428.
[2] KIVIMÄKI M, STRANDBERG T, PENTTI J, et al. Body-mass index and risk of obesity-related complex multimorbidity: an observational multicohort study. Lancet Diabetes Endocrinol. 2022;10(4):253-263.
[3] KOLIAKI C, LIATIS S, DALAMAGA M, et al. Sarcopenic Obesity: Epidemiologic Evidence, Pathophysiology, and Therapeutic Perspectives. Curr Obes Rep. 2019;8(4):458-471.
[4] JI T, LI Y, MA L. Sarcopenic Obesity: An Emerging Public Health Problem. Aging Dis. 2022;13(2):379-388.
[5] 李思远,宋娟,吴锦晖.肌少性肥胖与代谢综合征关系的研究进展[J].实用老年医学,2023,37(6):623-625.
[6] WANG H, HAI S, LIU YX, et al. Associations between Sarcopenic Obesity and Cognitive Impairment in Elderly Chinese Community-Dwelling Individuals. J Nutr Health Aging. 2019;23(1):14-20.
[7] 师燕,杨秋萍.肌少性肥胖发病机制的研究进展[J].中国临床研究, 2023,36(1):156-160.
[8] HONG SH, CHOI KM. Sarcopenic Obesity, Insulin Resistance, and Their Implications in Cardiovascular and Metabolic Consequences. Int J Mol Sci. 2020;21(2):494.
[9] DELLA GUARDIA L, SHIN AC. Obesity-induced tissue alterations resist weight loss: A mechanistic review. Diabetes Obes Metab. 2024;26(8): 3045-3057.
[10] PINEL A, GUILLET C, CAPEL F, et al. Identification of factors associated with sarcopenic obesity development: Literature review and expert panel voting. Clin Nutr. 2024;43(6):1414-1424.
[11] MIGLIAVACCA E, TAY SKH, PATEL HP, et al. Mitochondrial oxidative capacity and NAD+ biosynthesis are reduced in human sarcopenia across ethnicities. Nat Commun. 2019;10(1):5808.
[12] LAI Y, RAMÍREZ-PARDO I, ISERN J, et al. Multimodal cell atlas of the ageing human skeletal muscle. Nature. 2024;629(8010):154-164.
[13] AVESANI CM, DE ABREU AM, RIBEIRO HS, et al. Muscle fat infiltration in chronic kidney disease: a marker related to muscle quality, muscle strength and sarcopenia. J Nephrol. 2023;36(3):895-910.
[14] 赵旭冉,高金娥,娜日松,等.肌少症性肥胖与老年高血压的相关性临床研究[J].中华全科医学,2022,20(11):1874-1877.
[15] 翟兴月,韩云琰,周芸.肌少症性肥胖的发病机制及诊疗研究进展[J].肿瘤代谢与营养电子杂志,2023,10(5):579-584.
[16] 宋叶雨,范建高.少肌性肥胖合并脂肪性肝病的诊断与治疗[J].实用肝脏病杂志,2021,24(1):149-152.
[17] CRUZ-JENTOFT AJ, BAHAT G, BAUER J, et al. Sarcopenia: revised European consensus on definition and diagnosis. Age Ageing. 2019;48(1):16-31.
[18] FERNANDO P, BONEN A, HOFFMAN-GOETZ L. Predicting submaximal oxygen consumption during treadmill running in mice. Can J Physiol Pharmacol. 1993;71(10-11):854-857.
[19] 江涛,王新航,张露艺,等.中国老年人肌少症患病率的Meta分析[J].海南医学,2022,33(1):116-123.
[20] MINOR LK, ROTHBLAT GH, GLICK JM. Triglyceride and cholesteryl ester hydrolysis in a cell culture model of smooth muscle foam cells. J Lipid Res. 1989;30(2):189-197.
[21] HSU KJ, LIAO CD, TSAI MW, et al. Effects of Exercise and Nutritional Intervention on Body Composition, Metabolic Health, and Physical Performance in Adults with Sarcopenic Obesity: A Meta-Analysis. Nutrients. 2019;11(9):2163.
[22] 王继,张敏,李文博,等.有氧运动对2型糖尿病大鼠糖脂代谢、骨骼肌炎症和自噬的影响[J].中国组织工程研究,2024,28(8):1200-1205.
[23] AL SAEDI A, DEBRUIN DA, HAYES A, et al. Lipid metabolism in sarcopenia. Bone. 2022;164:116539.
[24] FRITZEN AM, LUNDSGAARD AM, KIENS B. Tuning fatty acid oxidation in skeletal muscle with dietary fat and exercise. Nat Rev Endocrinol. 2020;16(12):683-696.
[25] 徐婷,郭应坤,许华燕,等.磁共振成像在肌病中的临床应用研究进展[J].磁共振成像,2023,14(7):192-196+202.
[26] 王晓薇,许艳岚.WIF-1在COPD合并骨骼肌萎缩大鼠中的表达及其与血清炎症因子、Atrogin-1/MuRF-1蛋白水平的关系[J].临床和实验医学杂志,2024,23(1):1-5.
[27] 岳宁,易晓东,杨胜波.MuRF1和MAFbx/Atrogin-1的研究进展[J].四川解剖学杂志,2012,20(3):33-36+60.
[28] 王慧,罗勇.Atrogin-1和MuRF-1在肌肉萎缩中的作用机制及影响因素[J].实用医学杂志,2012,28(11):1921-1922.
[29] KIM S, YOU Y, KIM OK, et al. Silymarin Prevents High-Fat Diet-Induced Muscle Atrophy by Regulating Protein Degradation and Synthesis in Mice. J Med Food. 2022;25(7):793-796.
[30] PARK MJ, CHOI KM. Interplay of skeletal muscle and adipose tissue: sarcopenic obesity. Metabolism. 2023;144:155577.
[31] WANG L, VALENCAK TG, SHAN T. Fat infiltration in skeletal muscle: Influential triggers and regulatory mechanism. iScience. 2024;27(3): 109221.
[32] BATSIS JA, VILLAREAL DT. Sarcopenic obesity in older adults: aetiology, epidemiology and treatment strategies. Nat Rev Endocrinol. 2018; 14(9):513-537.
[33] YANG Y, ZHANG H, LI X, et al. Effects of PPARα/PGC-1α on the energy metabolism remodeling and apoptosis in the doxorubicin induced mice cardiomyocytes in vitro. Int J Clin Exp Pathol. 2015;8(10):12216-12224.
[34] 姚艳,王宗保,唐朝克.PPARs在长链脂肪酸调控能量代谢中的作用[J].生理科学进展,2016,47(1):1-6.
[35] 王慧婷,张岩晨,徐梦怡,等.能量代谢关键调控因子PGC-1α的研究进展[J].生理学报,2020,72(6):804-816.
[36] 高弘,李春,华玉涛,等.长链二元酸代谢中肉毒碱脂酰转移酶的作用[J].中国生物工程杂志,2003(6):14-16.
[37] JI S, YOU Y, KERNER J, et al. Homozygous carnitine palmitoyltransferase 1b (muscle isoform) deficiency is lethal in the mouse. Mol Genet Metab. 2008;93(3):314-322.
[38] KHAN AS, SUBRAMANIAM S, DRAMANE G, et al. ERK1 and ERK2 activation modulates diet-induced obesity in mice. Biochimie. 2017; 137:78-87.
[39] HUANG J, TAGAWA T, MA S, et al. Black Ginger (Kaempferia parviflora) Extract Enhances Endurance Capacity by Improving Energy Metabolism and Substrate Utilization in Mice. Nutrients. 2022;14(18):3845.
[40] MARCUS SL, MIYATA KS, ZHANG B, et al. Diverse peroxisome proliferator-activated receptors bind to the peroxisome proliferator-responsive elements of the rat hydratase/dehydrogenase and fatty acyl-CoA oxidase genes but differentially induce expression. Proc Natl Acad Sci U S A. 1993;90(12):5723-5727.
[41] AKBAR H, GRALA TM, VAILATI RIBONI M, et al. Body condition score at calving affects systemic and hepatic transcriptome indicators of inflammation and nutrient metabolism in grazing dairy cows. J Dairy Sci. 2015;98(2):1019-1032.
[42] TAO Z, ZHANG L, WU T, et al. Echinacoside ameliorates alcohol-induced oxidative stress and hepatic steatosis by affecting SREBP1c/FASN pathway via PPARα. Food Chem Toxicol. 2021;148:111956.
[43] ENKLER L, SZENTGYÖRGYI V, PENNAUER M, et al. Arf1 coordinates fatty acid metabolism and mitochondrial homeostasis. Nat Cell Biol. 2023;25(8):1157-1172.
[44] SZTALRYD C, KIMMEL AR. Perilipins: lipid droplet coat proteins adapted for tissue-specific energy storage and utilization, and lipid cytoprotection. Biochimie. 2014;96:96-101.

Aerobic exercise promotes remodeling of the energy metabolism network in the skeletal muscle of mice with sarcopenic obesity

PDF

Knowledge

Abstract

Cite this article

share this article

Figures/Tables 5

References

Related Articles 15

Recommended Articles

Metrics

Comments

[1]	Li Kaiying, Wei Xiaoge, Song Fei, Yang Nan, Zhao Zhenning, Wang Yan, Mu Jing, Ma Huisheng. Mechanism of Lijin manipulation regulating scar formation in skeletal muscle injury repair in rabbits [J]. Chinese Journal of Tissue Engineering Research, 2025, 29(8): 1600-1608.
[2]	Li Huayuan, Li Chun, Liu Junwei, Wang Ting, Li Long, Wu Yongli. Effect of warm acupuncture on PINK1/Parkin pathway in the skeletal muscle of rats with chronic fatigue syndrome [J]. Chinese Journal of Tissue Engineering Research, 2025, 29(8): 1618-1625.
[3]	Wang Xuanqiang, Zhang Wenyang, Li Yang, Kong Weiqian, Li Wei, Wang Le, Li Zhongshan, Bai Shi. Effects of chronic exposure to low-frequency pulsed magnetic fields on contractility and morphology of the quadriceps muscle in healthy adults [J]. Chinese Journal of Tissue Engineering Research, 2025, 29(8): 1634-1642.
[4]	Zhao Xiaoxuan, Liu Shuaiyi, Li Qi, Xing Zheng, Li Qingwen, Chu Xiaolei. Different exercise modalities promote functional recovery after peripheral nerve injury [J]. Chinese Journal of Tissue Engineering Research, 2025, 29(6): 1248-1256.
[5]	Zhang Wenhua, Li Xun, Zhang Weichao, Li Xinying, Ma Guoao, Wang Xiaoqiang . Promoting myogenesis based on the SphK1/S1P/S1PR2 signaling pathway: a new perspective on improving skeletal muscle health through exercise [J]. Chinese Journal of Tissue Engineering Research, 2025, 29(6): 1265-1275.
[6]	Wen Zixing, Xu Xin, Zhu Shengqun. Correlations between gastrocnemius morphology parameters and physical activity capacity in elderly females under high-frequency ultrasound [J]. Chinese Journal of Tissue Engineering Research, 2025, 29(5): 1058-1063.
[7]	Cai Zhixing, Xia Qiufang, Chen Lili, Zhu Danyang, Zhu Huiwen, Sun Yanan, Liang Wenyu, Zhao Heqian. Effect of Roujishuncuiyin on the improvement of skeletal muscle insulin resistance in a mouse model of type 2 diabetes mellitus [J]. Chinese Journal of Tissue Engineering Research, 2025, 29(35): 7537-7543.
[8]	Ji Long, Chen Ziyang, , Jin Pan, Kong Xiangkui, Pu Rui, . Lipophagy, exercise intervention and prevention and treatment of nonalcoholic fatty liver disease [J]. Chinese Journal of Tissue Engineering Research, 2025, 29(35): 7611-7619.
[9]	Liu Chenchen, Liu Ruize, Bao Mengmeng, Fang Li, Cao Liquan, Wu Jiangbo. Blood flow restriction training intervention in the elderly with sarcopenic obesity [J]. Chinese Journal of Tissue Engineering Research, 2025, 29(32): 6963-6970.
[10]	Wang Jiaqian, , Jiang Changjun, Peng Yi, Ma Mi, Li Junhan. Study on the role of aerobic exercise in regulating the CNPY2-mediated AKT/GSK3β pathway for improving non-alcoholic fatty liver [J]. Chinese Journal of Tissue Engineering Research, 2025, 29(30): 6441-6448.
[11]	Hu Shujuan, Liu Dang, Ding Yiting, Liu Xuan, Xia Ruohan, Wang Xianwang. Ameliorative effect of walnut oil and peanut oil on atherosclerosis [J]. Chinese Journal of Tissue Engineering Research, 2025, 29(30): 6482-6488.
[12]	Zhang Zihan¹, Wang Jiaxin¹, Yang Wenyi², Zhu Lei¹. Regulatory mechanism of exercise promoting mitochondrial biogenesis in skeletal muscle [J]. Chinese Journal of Tissue Engineering Research, 2025, 29(30): 6499-6508.
[13]	Liu Haowei, Tian Haodong, Huang Li, Yu Hanglin, Peng Li. Acute effects of blood flow restriction resistance exercise on serum metabolites in obese young men [J]. Chinese Journal of Tissue Engineering Research, 2025, 29(29): 6249-6259.
[14]	He Ningjuan, Li Li, Wang Su, Yang Jianshe, Lei Siyun, Wang Yang. Effects of aerobic or resistance exercise on hippocampal ras/Drebrin dendritic spine plasticity in a mouse model of Alzheimer’s disease [J]. Chinese Journal of Tissue Engineering Research, 2025, 29(26): 5528-5535.
[15]	Geng Longyu, Sheng Li, Bai Shuo, Gao Beiyao, Ge Ruidong, Jiang Shan . Role and molecular mechanism of pyroptosis in motor system diseases [J]. Chinese Journal of Tissue Engineering Research, 2025, 29(26): 5695-5703.