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作 者:郝丹丹 张垒 白春英[1] HAO Dandan;ZHANG Lei;BAI Chunying(Key Laboratory of Research on Human Genetic Disease at Universities of Inmer Mongolia Autonomous Region,Chifeng University Health Science Center,Chifeng 024000,China)
机构地区:[1]赤峰学院内蒙古人类遗传病研究重点实验室,024000 [2]赤峰学院附属医院神经外科
出 处:《中国糖尿病杂志》2025年第1期73-76,共4页Chinese Journal of Diabetes
基 金:国家自然科学基金(81860496);内蒙古自然科学基金(2022MS08032)。
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。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 NLRP3inflammasome to treat MAFLD-related liver fibrosis.
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