时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
More fundamentally, whether mitochondrial dysfunction initiates net proteolysis or merely reflects atrophy sequelae remains unresolved due to insufficient direct evidence.；Substantial controversy persists concerning the temporal pattern and dual functions of autophagy in sepsis-induced muscle atrophy—specifically, when its activity is protective as opposed to detrimental, and whether therapies should aim to stimulate or suppress it.；Such pretreatment strategies have limited clinical applicability, as the risk–benefit ratio of pharmacologically preventing sarcopenia in patients without a sepsis diagnosis remains unclear.
方法
Inclusion criteria were: (1) Study subjects were clinical patients or animal models diagnosed with sepsis/septic shock; (2) Study content was related to sarcopenia or muscle atrophy; (3) Literature published in English.；The methodological quality of the included studies was independently assessed by two reviewers using specific design tools, including the Cochrane Risk of Bias Assessment Tool (RoB-2.0) for randomized controlled trials (RCT),[21] the Newcastle-Ottawa scale (NOS) for clinical cohort studies (CS),[22] and the SYRCLE’s risk of bias tool for preclinical animal studies.[23] Any disagreements during the quality assessment process are resolved through discussion or arbitration by a third adjudicator.；Due to the challenges of obtaining muscle biopsies from septic patients, only a few human studies have reliably confirmed three core pathological changes: UPS activation,[24] inflammatory cell infiltration,[25] and ERS.[26] Most proposed mechanisms derive from rodent models and in vitro studies, with a scarcity of high-quality human data.
核心结论
This review will critically synthesize current knowledge on SASP pathogenesis, measuring parameters and interventions, and conclude with a critical appraisal of research limitations and future directions to provide insightful perspectives.Methods and Search StrategyA systematic search strategy was employed to comprehensively collect relevant literature.；Functionally, these mitochondria demonstrate markedly enhanced oxidative stress—characterized by elevated ROS and MDA alongside reduced antioxidants like SOD, CAT, and GPX—as well as decreased ATP production and Ca2+ overload.；During sepsis, impaired mitochondrial membrane potential,[51] reduced electron transport chain (ETC) complex I–IV activities,[27,31,33] and increased proton leak collectively[52] diminish ATP output.[37,53,54] This bioenergetic deficit directly contributes to muscle weakness and impaired mobility.
局限
This review will critically synthesize current knowledge on SASP pathogenesis, measuring parameters and interventions, and conclude with a critical appraisal of research limitations and future directions to provide insightful perspectives.Methods and Search StrategyA systematic search strategy was employed to comprehensively collect relevant literature.；However, this field faces significant limitations, as only a single clinical study has thus far confirmed ERS marker upregulation in the rectus abdominis muscle of septic patients,[26] while the remaining mechanistic evidence comes entirely from preclinical models, creating a substantial gap in human tissue validation.；However, findings regarding MSTN inhibition remain inconsistent, as YK11 and antisense MSTN administration ameliorate SASP, but genetic deficiency of MSTN does not confer protection.
对本项目的价值
中高价值：属「衰老细胞清除 / SASP 轴」方向；细胞衰老 / senolytics / SASP栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.1/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 80,191 字符，题名指纹 0.8，已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：脓毒症相关肌少症：机制与治疗的新认识
- 英文标题：Sepsis-associated sarcopenia: Emerging insights into mechanisms and therapeutic approaches.
- 期刊与标识：Journal of intensive medicine · PMID 42979105 · DOI 10.1016/j.jointm.2026.03.005 · PMC PMC13728391