数据日期 2026-10-29 · 生成时间 2026-10-29 06:03
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。
研究问题
Excess lipid accumulation and a sedentary lifestyle are associated with metabolic dysfunction-associated fatty liver disease (MAFLD), but the causal mechanisms and preventive methods are not fully understood.
方法
Macroautophagy/autophagy is a lysosomal degradation pathway robustly induced by exercise and plays a key role in lipid metabolism.
核心结论
Understanding the mechanisms by which exercise activates autophagy and elicits metabolic benefits in the liver will provide important insights into the pathogenesis of MAFLD.；Here, we discovered negative correlations between expression and lactylation of WDR41 (WD repeat domain 41) and pathogenesis of a series of human hepatic metabolic diseases.；We found that WDR41 was a pro-autophagy protein that underwent lactylation in response to autophagy-inducing conditions, such as exercise.；WDR41 was lactylated at lysine 319 (K319), a modification facilitated by LDHA (lactate dehydrogenase A) upon autophagy induction, and delactylated by SIRT2 (sirtuin 2). ‖ 结论：Thus, we demonstrated that WDR41 lactylation at K319 is an important regulatory mechanism by which exercise regulates autophagy and hepatic glucose and lipid metabolism.
局限
未能获取全文，具体设计细节、失访与统计学处理无法核验。
对本项目的价值
★★★☆☆ 代谢轴既干预敏感性最高，也是老药新用供给最充足的来源。
原文题录
- 英文标题：Exercise-induced lactylation in WDR41 initiates autophagy and improves fatty liver diseases.
- 期刊与标识：Autophagy · PMID 42946691 · DOI 10.1080/15548627.2026.2754683**
A 级证据分级：A 级（同行评议人体研究）
本文属人体研究证据，但需注意：观察性或小样本干预的结论不等于已证实临床获益；效应量与长期安全性仍需更大规模、更长随访的试验验证。
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」（SOP §4.2 摘要级）撰写，依据期刊公开摘要与 PubMed 元数据；付费墙全文未获取之处已标注「待补全文」，未做任何数值推算补全。