单核/巨噬细胞调控心梗后心肌纤维化的研究进展  

Progress in monocytes/macrophages regulating cardiac fibrosis after myocardial infarction

作　　者：覃宇燕 吴茜 余细勇 QIN Yu-yan;WU Qian;YU Xi-yong(School of Pharmaceutical Sciences,Guangzhou Medical University,Guangdong Provincial Key Laboratory of Molecular Target&Clinical Pharmacology,Guangzhou 511436,China)

机构地区：[1]广州医科大学药学院,广东省分子靶标与临床药理学重点实验室,广东广州511436

出　　处：《中国病理生理杂志》2020年第8期1521-1525,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.81330007,No.U1601227);广东省科技计划项目(No.2015B020225006);广州市教育局专项资助(No.201831836)。

摘　　要：急性心肌梗死(acute myocardial infarction,AMI)是一种严重的缺血性心脏病,持续的心肌缺血可导致心肌细胞大量凋亡或坏死而丢失。心肌纤维化(myocardial fibrosis,MF)是指在心肌的正常组织结构中胶原纤维过量积聚、心脏组织中胶原浓度显著升高或胶原成分发生激剧改变,导致心脏僵硬度增加、心功能下降。MF是心肌梗死的主要病理生理学过程,可导致心脏重构(cardiac remodeling),并逐渐发展为慢性心力衰竭(chronic heart failure,CHF)[1]。Myocardial fibrosis is the main pathophysiology following myocardial infarction,which leads to cardiac remodeling and heart failure ultimately. The inflammatory response of monocyte/macrophage recruitment is essential to heart repair after myocardial infarction. However,macrophages in different periods after myocardial infarction are multifaceted,and participate in the process of myocardial fibrosis. This article mainly elucidates the relationship between monocytes/macrophages and cardiac fibrosis after myocardial infarction.

关 键 词：单核/巨噬细胞 心肌梗死 心肌纤维化 

分 类 号：R542.2[医药卫生—心血管疾病] R363.2[医药卫生—内科学]