Department of Orthopedics, Xiangya Hospital, Central South University, Changsha 410008, China.
National Clinical Research Center for Geriatric Disorders, Central South University, Xiangya Hospital, Changsha 410008, China.
Cells. 2022 Mar 23;11(7):1078. doi: 10.3390/cells11071078.
With global ageing, sarcopenia, as an age-related disease, has brought a heavy burden to individuals and society. Increasing attention has been given to further exploring the morbidity mechanism and intervention measures for sarcopenia. Pyroptosis, also known as cellular inflammatory necrosis, is a kind of regulated cell death that plays a role in the ageing progress at the cellular level. It is closely related to age-related diseases such as cardiovascular diseases, Alzheimer's disease, osteoarthritis, and sarcopenia. In the process of ageing, aggravated oxidative stress and poor skeletal muscle perfusion in ageing muscle tissues can activate the nod-like receptor (NLRP) family to trigger pyroptosis. Chronic inflammation is a representative characteristic of ageing. The levels of inflammatory factors such as TNF-α may activate the signaling pathways of pyroptosis by the NF-κB-GSDMD axis, which remains to be further studied. Autophagy is a protective mechanism in maintaining the integrity of intracellular organelles and the survival of cells in adverse conditions. The autophagy of skeletal muscle cells can inhibit the activation of the pyroptosis pathway to some extent. A profound understanding of the mechanism of pyroptosis in sarcopenia may help to identify new therapeutic targets in the future. This review article focuses on the role of pyroptosis in the development and progression of sarcopenia.
随着全球老龄化的到来，作为一种与年龄相关的疾病，肌少症给个人和社会带来了沉重的负担。人们越来越关注进一步探索肌少症的发病机制和干预措施。细胞焦亡又称细胞炎性坏死，是一种在细胞水平上参与衰老进程的调控性细胞死亡。它与心血管疾病、阿尔茨海默病、骨关节炎和肌少症等与年龄相关的疾病密切相关。在衰老过程中，衰老肌肉组织中氧化应激加重和骨骼肌灌注不良可激活核苷酸结合寡聚化结构域样受体（NLR）家族，引发细胞焦亡。慢性炎症是衰老的一个代表性特征。TNF-α 等炎症因子的水平可能通过 NF-κB-GSDMD 轴激活细胞焦亡的信号通路，这仍有待进一步研究。自噬是维持细胞内细胞器完整性和细胞在逆境中存活的一种保护机制。骨骼肌细胞的自噬可以在一定程度上抑制细胞焦亡途径的激活。深入了解细胞焦亡在肌少症中的作用机制，可能有助于未来确定新的治疗靶点。本文综述了细胞焦亡在肌少症发生发展中的作用。
