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线粒体 DNA 可激活非酒精性脂肪性肝病中的 AIM2 炎性体并诱导肝细胞发生细胞焦亡。

Mitochondrial DNA enables AIM2 inflammasome activation and hepatocyte pyroptosis in nonalcoholic fatty liver disease.

机构信息

Department of Hepatopancreatobillary Surgery, Xuzhou City Cancer Hospital, Xuzhou, Jiangsu, China.

Class 182, Queen Mary School, Nanchang University, Nanchang, Jiangxi, China.

出版信息

Am J Physiol Gastrointest Liver Physiol. 2021 Jun 1;320(6):G1034-G1044. doi: 10.1152/ajpgi.00431.2020. Epub 2021 Mar 17.

DOI:10.1152/ajpgi.00431.2020
PMID:33728991
Abstract

Mitochondria damage exacerbates NAFLD through trigerring AIM2 inflammasome activation and hepatocyte pyroptosis. This study provides novel insights into the underlying mechanisms of mitochondrial DNA synthesis in NAFLD and also suggests potential therapeutic targets for the treatment of NAFLD.

摘要

线粒体损伤通过触发 AIM2 炎性小体激活和肝细胞焦亡加剧非酒精性脂肪性肝病。本研究为非酒精性脂肪性肝病中线粒体 DNA 合成的潜在机制提供了新的见解，并为非酒精性脂肪性肝病的治疗提供了潜在的治疗靶点。

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