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
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摘要（PubMed 原文节选）
Mitochondrial dysfunction is frequently well-known to induce mitochondrial dysfunction-associated senescence (MIDAS), a specialized form of cellular senescence marked by a distinct senescent phenotype. Sirtuin-3 (SIRT3) is a key regulator of mitochondrial function through its deacetylase activity, and emerging evidence highlights that its deficiency induces MIDAS in fibroblasts. However, the precise mechanism by which SIRT3 regulates MIDAS, as well as the role of MIDAS in tumorigenesis, remains incompletely understood. Here, we report that SIRT3 deficiency inhibits colorectal cancer (CRC) progression by inducing MIDAS. Mechanistically, SIRT3 deacetylates the mitochondrial carrier SLC25A13 at…
对本项目的价值
中等价值：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 2.2/5（★★☆☆☆）
全文不可及原因
无 PMCID 且 OpenAlex / Unpaywall 未提供可下载 OA PDF
原文题录
- 中文题名：SIRT3 缺失经 SLC25A13 乙酰化触发线粒体功能障碍相关衰老，抑制结直肠癌进展
- 英文标题：SIRT3 deficiency triggers mitochondrial dysfunction-associated senescence to suppress colorectal cancer progression via SLC25A13 acetylation.
- 期刊与标识：Oncogene · PMID 42966746 · DOI 10.1038/s41388-026-04037-8 · EDAT 2026-11-01