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
Studies have shown that the levels of p62 and LC3-II in Sidt2-knockout hepatocytes were significantly increased, indicating that a large number of autophagosomes were accumulated without degradation, and the content of mature cathepsin B…；This state blocks autophagosome-lysosomal fusion, which in turn weakens the efficiency of fatty acid β -oxidation, leading to abnormal accumulation of lipid droplets in hepatocytes and accelerating the progression of MASLD ( ).
方法
（原文未给出可直接抽取的对应表述）
核心结论
Similarly, by inhibiting the localization and activity of mTORC1 on lysosomes, nuciferine and polydatin activated TFEB-mediated ALP activity and reduced hepatic lipid accumulation, which significantly improved hepatic steatosis, inflammation and hepatocyte…；Clinical studies have shown that compared with adjacent non-tumor tissues, the expression of LC3-II in HCC tumor tissues is significantly increased and the expression of p62 is decreased, indicating that autophagy activity is enhanced, and it is positively…；Mechanistically, HCC cells up-regulate autophagy to cope with high metabolic needs and increased oxidative stress associated with rapid proliferation, forming a dependence on autophagic flux to gain survival advantages.
局限
（原文未给出可直接抽取的对应表述）
对本项目的价值
人群纵向证据，可用于假说生成与终点选择：代谢—器官轴是干预安全性的主要约束面。 ｜ 价值分 1.9/5（★★☆☆☆）
全文来源
PubMed PMC JATS 全文（正文 65,692 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：Autophagy-lysosome pathway dysfunction in MASLD progression: molecular mechanisms and therapeutic targets.
- 期刊与标识：Frontiers in medicine · PMID 42953075 · DOI 10.3389/fmed.2026.1961366
B 级证据分级：B 级（同行评议临床前研究，主要为动物模型）
本文核心结论来自动物模型或体外细胞学，属临床前证据，不能外推至人体。「延长健康寿命」「改善功能」等表述在小鼠中的意义，与人类临床结局之间仍有距离。
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