ApoA-I在结核病形成中的潜在作用及机制研究  

The Potential Role and Mechanism of ApoA-I in the Formation of Tuberculosis

作　　者：贾晨曦 刘麒苗 武琛佳 王昕 郝明媛 董丽 JIA Chenxi;LIU Qimiao;WU Chenjia;WANG Xin;HAO Mingyuan;DONG Li(Institutes of Biomedical Sciences Shanxi University,Taiyuan 030006,China)

机构地区：[1]山西大学生物医学研究院,太原030006

出　　处：《中国细胞生物学学报》2024年第6期1211-1219,共9页Chinese Journal of Cell Biology

基　　金：山西省重点研发计划(批准号:202102130501009);呼伦贝尔市科技计划(批准号:SF2023015)资助的课题。

摘　　要：结核病(tuberculosis,TB)主要是由结核分枝杆菌(Mycobacterium tuberculosis,Mtb)引起的免疫病理损伤并以干酪样肉芽肿为特征性病变的传染性疾病,其病理发生机制较为复杂。载脂蛋白A1(Apolipoprotein A1,ApoA-I)是血浆中运载脂质的非糖基化蛋白质,具有抗炎、抗氧化、调节胆固醇运输和调节细胞自噬等功能,参与多种疾病形成。近年来,ApoA-I与结核病的关联受到广泛关注,该文将对ApoA-I在结核病形成中的作用及其生物学机制加以综述,为完善结核病的发病机理以及探索治疗结核病的新方向提供科学依据。Tuberculosis,induced by Mtb(Mycobacterium tuberculosis),is characterized by caseating granuloma formation in response of immunopathological damages.The molecular mechanism underlying the tuberculosis is complex.ApoA-I(Apolipoprotein A1),as a non-glycosylated plasma protein,is anti-inflammatory and antioxidant,able to regulate cholesterol transport,and autophagy,to be involved in various other diseases.The association between ApoA-I and pathogenesis of tuberculosis has attracted extensive attention lately.This article will review the role of ApoA-1 in the tuberculosis development and related biological signaling pathway,which will complete the pathogenesis of tuberculosis and provide a clue for possible strategy of treatment for tuberculosis.

关 键 词：载脂蛋白A1 结核病 分子机制 

分 类 号：R52[医药卫生—内科学]