时间标签：数据日期 2026-11-03 · 生成时间 2026-11-03 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/31 – 2026/11/03 ｜ 情报发生日期 2026-11-03
证据级别：摘要级。本条依据 PubMed 结构化摘要与元数据撰写，付费墙全文未获取、未逐节核验，本站未做任何数值推算补全。
摘要（PubMed 原文节选）
Aging is a universal biological process signified by a time-dependent decline in physiological activity, driven by molecular and cellular damage, leading to greater susceptibility to diseases and fatal outcomes. Impaired proteostasis is a key aspect of cellular aging in which the cells become less efficient at folding, repairing, and recycling proteins, consequently inducing accumulation of damaged and aggregation-prone proteins. The onset of muscle loss is driven by a reduction in protein synthesis, heightened activation of proteolytic pathways, and elevated ER stress factors, collectively contributing to functional decline and increased vulnerability with aging. Muscle atrophy, whether age…
对本项目的价值
中等价值：属「营养感知—自噬—蛋白稳态轴」方向；肌肉骨骼 / 衰弱 / 肌少症栏目可用作本项目文献库与综述素材。 ｜ 价值分 2.6/5（★★★☆☆）
全文不可及原因
标注 OA 但 PDF 下载失败或未通过题名指纹归属校验
原文题录
- 中文题名：衰老骨骼肌蛋白稳态网络失调：肌少症与肌肉消耗的机制与治疗靶点
- 英文标题：Proteostasis network dysregulation in aging skeletal muscle: Mechanisms and therapeutic targets in sarcopenia and muscle wasting.
- 期刊与标识：Exp Gerontol · PMID 42966421 · DOI 10.1016/j.exger.2026.113373 · EDAT 2026-10-31