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
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）
Intervertebral disc degeneration (IDD) is a major cause of chronic low back pain, and excessive mechanical stress is considered an important driver of nucleus pulposus cell (NPC) dysfunction. However, the molecular mechanisms linking mechanotransduction to mitochondrial injury and protein homeostasis remain incompletely understood. In thi…
对本项目的价值
参考价值：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 1.8/5（★★☆☆☆）
全文不可及原因
无 PMCID 且 Europe PMC / OpenAlex / Unpaywall 未提供可下载 OA 全文
原文题录
- 中文题名：机械应力经 PIEZO1-YAP1/TEAD1 介导 NEDD4 激活与 NFS1 泛素化依赖线粒体功能障碍加速椎间盘退变
- 英文标题：Mechanical stress accelerates intervertebral disc degeneration through PIEZO1-YAP1/TEAD1-mediated NEDD4 activation and NFS1 ubiquitination-dependent mitochondrial dysfunction.
- 期刊与标识：Biochimica et biophysica acta. Molecular basis of disease · PMID 42971267 · DOI 10.1016/j.bbadis.2026.168522