脂噬抑制细胞泡沫化在动脉粥样硬化中作用的研究进展  被引量:3

Role of inhibition of cellular foaming by lipophagy in atherosclerosis

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作  者:靳雅 张立双[2] 黄湘龙 马耀磊 刘金杰 张晗[1] 李霄[1] JIN Ya;ZHANG Lishuang;HUANG Xianglong;MA Yaolei;LIU Jinjie;ZHANG Han;LI Xiao(State Key Laboratory of Component-based Chinese Medicine,Key Laboratory of Pharmacology of Traditional Chinese Medical Formulae,Ministry of Education,Institute of Traditional Chinese Medicine,Tianjin University of Traditional Chinese Medicine,Tianjin 301617,China;Tianjin Binhai New Area Hospital of Traditional Chinese Medicine and the Fourth Affiliated Hospital of Tianjin University of Traditional Chinese Medicine,Tianjin 300451,China)

机构地区:[1]天津中医药大学组分中药国家重点实验室,方剂学教育部重点实验室,中医药研究院,天津301617 [2]天津市滨海新区中医医院暨天津中医药大学第四附属医院,天津300451

出  处:《中国病理生理杂志》2024年第3期564-571,共8页Chinese Journal of Pathophysiology

基  金:天津市教委科研计划项目(No.2023KJ137)。

摘  要:动脉粥样硬化(atherosclerosis,AS)是多数心脑血管疾病致死的重要原因之一。全球疾病研究表明,AS性心脏病在全球流行,发病数已由1990年的约1亿例增长为2019年的1.8亿例[1];在2020年流行病调查中发现30岁以上颈动脉内膜增厚的比率为27.6%[2]。同时,国家心血管病中心发布的《中国心血管健康与疾病报告2021》中指出我国心血管病人数达3.3亿,每5例死亡中就有2例死于心血管病。AS是一种以动脉血管壁脂质异常蓄积为主要特征的慢性血管炎症性病变,形成富含脂质的泡沫细胞(foam cells)是AS病变的起始与早期重要病理特征之一(图1)。Atherosclerosis is a chronic vascular inflammatory disease caused by abnormal lipid metabolism.The formation of lipid-rich foam cells acts as the initial trigger for development of atherosclerotic lesions.Recent studies have shown that lipophagy,a form of selective autophagy,can selectively degrade lipid droplets stored intracellularly and promote cholesterol efflux through the autophagic lysosomal pathway.As a result,intracellular lipid accumulation is re duced and foaming is inhibited,making lipophagy a potential new target for current anti-atherosclerosis therapy.This arti cle reviews the crucial role and molecular mechanism of lipophagy in the link between lipid metabolism and atherosclero sis.Its objective is to outline the regulatory mechanism of lipophagy and present fresh insights for the treatment of athero sclerotic diseases.

关 键 词:动脉粥样硬化 脂噬 自噬 脂质代谢 

分 类 号:R589.2[医药卫生—内分泌] R363.2[医药卫生—内科学] R972.6[医药卫生—临床医学]

 

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