时间标签：数据日期 2026-11-01 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/31–2026/11/01 ｜ 情报发生日期 2026-11-01
研究问题
Therapeutic interventions targeting mitochondrial dysfunction and advanced metabolism The drug development paradigm for MASLD has undergone a profound shift: From early ‘peripheral empirical antioxidation’ to modern ‘precise energy…；To provide a rigorous clinical and translational perspective, contemporary therapeutic strategies must be strictly evaluated based on their evidence‑graded clinical stages and mechanistic boundaries (Table II).
方法
（原文未给出可直接抽取的对应表述）
核心结论
While systemic drivers reduce intrahepatic lipid partly through weight loss and improved peripheral metabolism, their direct long‑term effects on hepatocyte organelle quality control require longitudinal study.
局限
The heterogeneity of formulations, doses and study models precludes assigning a single validated SIRT1/AMPK/Smad3/microRNA‑141 mechanism to its effects in human MASH.；The sequence is a conceptual framework and does not establish a universal linear NRF2‑to‑antioxidant‑exhaustion pathway in human MASH.
对本项目的价值
综述级证据，用于快速对齐领域共识与空白：线粒体是衰老干预的共同下游效应器，可用于跨器官效应的统一读数。 ｜ 价值分 1.7/5（★★☆☆☆）
全文来源
出版商 OA PDF（正文 62,861 字符，已过 DOI 逐字 + 题名指纹双重归属校验）
原文题录
- 英文标题：Mitochondrial dysfunction in metabolic dysfunction-associated steatotic liver disease: Mechanistic insights and therapeutic horizons (Review).
- 期刊与标识：Molecular medicine reports · PMID 42960447 · DOI 10.3892/mmr.2026.14055
C 级证据分级：C 级（预印本 / 观点评论，非原始研究）
本文属观点/评论类文献，不是原始研究。其论点依赖于作者对既有证据的梳理与判断，不构成新的实验证据。本站标注 C 级即为此意——阅读时请把它当作「领域内的思考框架」，而非「研究发现」。
关于本文的文献来源：本站依据 IMA 知识库「五刊监控·深度文献卡片」撰写，依据已获取的期刊全文（方法、样本量与结论已回到原文核对）；未能获取全文的同批条目另行标注「摘要级」，全程未做任何数值推算补全。