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
Mechanistically, TNFAIP3 mitigates hepatic lipid accumulation by deubiquitinating ATG4B, thereby promoting autophagic flux.；These findings delineate a previously unrecognized NF-κB-TNFAIP3 axis that may serve as a potential therapeutic target for MASLD.
方法
Western blot analysis Total protein extraction from HepG2 cells or mouse liver tissues was performed by lysing the samples in RIPA buffer supplemented with protease and phosphatase inhibitors on ice.；According to the degree of fatty infiltration in the adjacent liver tissue, the samples were divided into two groups: a control group with minimal or absent steatosis, and a hepatic steatosis group.；Prediction of potential ubiquitination sites on ATG4B was performed using the GPS-Uber database, which evaluates lysine residues for putative ubiquitination based on sequence motifs and scoring thresholds.
核心结论
Consistent with this finding, we observed that HF diet significantly impaired insulin sensitivity and glucose regulation, whereas TNFAIP3 overexpression ameliorated these abnormalities and reduced insulin levels.；Moreover, TNFAIP3 overexpression significantly increased LC3-II levels and decreased p62 expression, indicating enhanced autophagic activity.；These results suggest reduced lipogenesis and improved cellular metabolic homeostasis (Fig. ).；We found that either knockdown of ATG4B or TNFAIP3 resulted in increased lipid droplet accumulation, whereas either overexpression of ATG4B or TNFAIP3 attenuated this phenotype (Supplementary Fig. , Fig. , Supplementary Fig. ).；Thus, the NF-κB-TNFAIP3 feedback loop in hepatocytes may represent a potential therapeutic target for MASLD. conclusion of the experimental period, after a 12 h overnight fast, the mice were euthanized.
局限
Therefore, it remains to be further investigated whether the NF-κB-TNFAIP3 feedback loop plays distinct roles in different hepatic cell types (hepatocytes and non-parenchymal cells), tissues (adipose tissue, intestine, liver), or in the…；This present study still has several limitations.
对本项目的价值
临床前机制证据，需评估物种外推与剂量可行性：代谢—器官轴是干预安全性的主要约束面。 ｜ 价值分 3.2/5（★★★☆☆）
全文来源
PubMed PMC JATS 全文（正文 45,391 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：The NF-κB-TNFAIP3 axis attenuates MASLD via activation of hepatocyte autophagy.
- 期刊与标识：Cell death discovery · PMID 42957644 · DOI 10.1038/s41420-026-03310-9
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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