血管紧张素信号调控心肌纤维化的研究进展  

Research Progress of Angiotensin Signaling in Regulating Myocardial Fibrosis

作　　者：张宏檑 徐嘉荇 李雯婷 刘康[1] ZHANG Honglei;XU Jiaxing;LI Wenting;LIU Kang(Department of Traditional Chinese Medicine,China Pharmaceutical University,Nanjing 211198,China;不详)

机构地区：[1]中国药科大学中药学院,江苏南京211198

出　　处：《中外医学研究》2024年第32期180-184,共5页CHINESE AND FOREIGN MEDICAL RESEARCH

基　　金：国家自然科学基金面上项目(82174009)。

摘　　要：心肌纤维化被认为是多种心血管疾病进入终末期的病理过程,可导致心脏舒缩功能受损、心律失常、心力衰竭甚至心源性猝死。由于参与心肌纤维化的细胞类型及信号通路的复杂性,目前仍缺乏理想的治疗方法抑制或逆转心肌纤维化。肾素-血管紧张素-醛固酮系统的异常激活被认为是导致不良心肌重构的主要病理机制之一,本文聚焦于血管紧张素信号转导通路与心肌纤维化的关系进行综述,期望为临床心肌纤维化治疗策略提供更多的选择。Myocardial fibrosis is a common pathological process of various cardiovascular diseases,ultimately leading to systolic and diastolic dysfunction,arrhythmia,heart failure,and even sudden cardiac death.Due to the intricate nature of the heart cell types and signaling pathways involved in myocardial fibrosis,there remains a lack of ideal therapies for preventing or reversing myocardial fibrosis.The abnormal activation of the renin-angiotensin-aldosterone system is a major pathological mechanism contributing to adverse myocardial remodeling.This review specifically focuses on the relationship between the angiotensin signal transduction pathway and myocardial fibrosis,hoping to provide more choices for the clinical therapy of myocardial fibrosis.

关 键 词：心肌纤维化 肾素-血管紧张素-醛固酮系统 血管紧张素Ⅱ 血管紧张素1-7 血管紧张素转换酶2 

分 类 号：R542.2[医药卫生—心血管疾病]