NOD样受体家族Pyrin域蛋白3炎性小体对代谢相关脂肪性肝病肝纤维化机制的研究进展
Research progress of targeting NOD-like receptor family Pyrin domain containing 3 inflammasome for the treatment of experimental MAFLD-associated liver fibrosis
郝丹丹 1张垒 2白春英1
作者信息
- 1. 024000 赤峰学院内蒙古人类遗传病研究重点实验室
- 2. 赤峰学院附属医院神经外科
- 折叠
摘要
代谢相关脂肪性肝病(MAFLD)是患者肝纤维化的主要病因.NOD样受体家族Pyrin域蛋白3(NLRP3)炎性小体激活是MAFLD相关肝纤维化发展的关键因素.本文综述NLRP3炎性小体激活,促进MAFLD相关肝纤维化进展的机制,并介绍靶向抑制NLRP3 炎性小体,治疗MAFLD相关肝纤维化的药理机制.
Abstract
Metabolic dysfunction-associated fatty liver disease(MAFLD)is becoming an leading causes of hepatic fibrosis worldwide,resulting in MAFLD-related liver fibrosis.Emerging evidences have indicated that the activation of the NOD-like receptor family Pyrin domain containing 3(NLRP3)inflammasome is a critical contributor to the development of MAFLD-related liver fibrosis.This article reviews the mechanism by which NLRP3 inflammasome activation promotes the development of MAFLD-related liver fibrosis,and focuses on the pharmacological mechanism of drugs targeting NLRP3 inflammasome to treat MAFLD-related liver fibrosis.
关键词
代谢相关脂肪性肝病/肝纤维化/炎性小体Key words
Metabolic dysfunction-associated fatty liver disease/Liver fibrosis/Inflammasome引用本文复制引用
出版年
2025
NETL
NSTL
万方数据