摘要
早期生长反应蛋白1(EGR1)属于即刻早期基因家族,是重要核转录因子,参与调控多种蛋白。EGR1在各种刺激下可快速诱导表达,参与丝裂原活化蛋白激酶等通路的下游信号转导,与细胞增殖分化与凋亡、组织损伤、再生修复等的调控机制密切相关。EGR1参与肝再生、细胞生长分化和细胞凋亡等生物学功能,并参与肝纤维化、胆汁淤积性肝病、酒精性脂肪肝和肝癌等病理生理机制。EGR1可能改善肝病的病理病变,也可能加速病情发展,其机制可能涉及EGR1的负反馈调节及其下游靶基因发挥的功能等。关注EGR1在临床研究的调控机制,旨在为探寻肝病的治疗靶点提供新线索。
Early growth response factor protein 1(EGR1),a member of the immediate early gene family,is an important nuclear transcription factor involved in the regulation of various proteins.EGR1 can be rapidly induced and expressed when stimulated by various factors participate in the downstream signal transduction of signaling pathways,such as mitogen-activated protein kinase pathways,which is closely related to cell proliferation,differentiation,apoptosis,tissue damage,and regeneration repair.The biological functions of EGR1 are manifested by its involvement in liver regeneration,cell growth and differentiation,and cell apoptosis,and its pathophysiological mechanisms are possibley related to liver fibrosis,cholestatic liver disease,alcoholic fatty liver and hepatocellular carcinoma.EGR1 can improve the pathological changes in liver disease.Meanwhile,it can also accelerate the progression of liver disease.The negative feedback regulation mechanism of EGR1 and the diverse functions of its downstream target genes may play a role in these pathways.This paper focuses on the regulatory mechanism of EGR1 in clinical research,and is expected to offer some novel clues to the investigation of the therapeutic targets in liver diseases.
作者
曾伟兰
汪艳
ZENG Wei-lan;WANG Yan(School of Pharmaceutical Science,Southern Medical University,Guangzhou 510515,China;Biomedical Research Center,Southern Medical University,Guangzhou 510515,China;Guangdong Provincial Research Institute of Liver Fibrosis,Guangzhou 510515,China)
出处
《中国药理学与毒理学杂志》
CAS
北大核心
2020年第9期702-712,共11页
Chinese Journal of Pharmacology and Toxicology
基金
国家自然科学基金(81670522)
国家自然科学基金(82070589)
深圳市“三名工程项目”(SZSM201911001)
南方医科大学南方医院院长基金(2018Z016)。
关键词
早期生长反应蛋白1
肝再生
肝损伤
early growth response factor protein 1
liver regeneration
liver damage