缺氧诱导因子-1α参与肝纤维化形成机制研究进展  

Mechanism of hypoxia inducible factor-1αinvolving in liver fibrosis

作　　者：刘瑞清(综述) 袁小澎(审校)[1] Liu Ruiqing;Yuan Xiaopeng(Division of Laboratory Medicine,Zhujiang Hospital,Southern Medical University,Guangzhou 510515,Guangdong Province,China)

机构地区：[1]南方医科大学珠江医院检验医学部,广州市510515

出　　处：《实用肝脏病杂志》2021年第1期145-148,共4页Journal of Practical Hepatology

基　　金：国家自然科学基金资助项目(编号:30972788)。

摘　　要：目的肝纤维化是一种由于反复肝损伤而导致肝组织细胞外基质过多沉积导致的疾病。缺氧损伤为肝损伤的一部分,缺氧诱导因子-1α(HIF-1α)是响应缺氧应激的关键转录因子,在肝纤维化组织和活化的肝星状细胞(HSC)表达显著增加。目前,通过对大量HIF-1α依赖性基因和信号通路的研究,确认这些基因及其通路的变化参与肝纤维化发展过程,并可能在肝纤维化发生发展过程中起关键作用。本文综述了HIF-1α相关的信号通路参与肝纤维化发展的相关机制,并对上游影响HIF-1α合成和降解的相关信号通路进行了阐述,为其作为新型治疗靶点的可能潜力提供依据。Objective Liver fibrosis is caused by excessive deposition of extracellular matrix in liver tissues due to repeated liver injuries and hypoxia injury is a part of liver injury.Hypoxia inducible factor-1α(HIF-1α)is a key transcription factor in response to hypoxia stress,and its expression in liver fibrotic tissues and activated HSCs is significantly increased.At present,a number of HIF-1αdependent genes and related signaling pathways have been studied to confirm that the changes of these genes and pathways are related to the development of liver fibrosis,suggesting that HIF-1αmay play a key role in liver fibrosis.In this review,the mechanism of HIF-1α-related signaling pathway in the development of liver fibrosis and the synthesis and degradation of HIF-1αfrom the upstream are described.

关 键 词：肝纤维化 缺氧诱导因子-1Α 治疗靶点 

分 类 号：R73[医药卫生—肿瘤]