细胞学机制在调控心肌梗死后炎症反应中的研究进展  

Cytological Mechanisms in Regulation of Post-infarction Inflammatory Response

作　　者：王茜 李晶洁[1] WANG Qian;LI Jingjie(Department of Cardiology,The First Affiliated Hospital of Harbin Medical University,Harbin 150000,Heilongjiang,China)

机构地区：[1]哈尔滨医科大学附属第一医院心内科,黑龙江哈尔滨150000

出　　处：《心血管病学进展》2020年第2期190-192,共3页Advances in Cardiovascular Diseases

基　　金：哈尔滨市应用技术研究与开发项目基金(2017RAXQJ068)。

摘　　要：炎症在心肌梗死后心脏修复中发挥重要作用,适度的炎症反应可以缩小梗死范围,促进缺血心肌的恢复,而持久激活的炎症反应则会加重缺血损伤,引起心脏不良重构。最近研究表明,心肌梗死后炎症和修复细胞的功能超出了传统学说所提出的作用范围。现就梗死后炎症反应的细胞学机制的研究进展做一综述,为进一步研究如何通过调控心肌梗死后的炎症反应从而抑制病理性重构为临床治疗提供新的方向。Inflammation plays a crucial role in cardiac repair after myocardial infarction.Moderate inflammatory response can reduce the infarct size and promote recovery of ischemic myocardium,while excessive inflammation will aggravate ischemic injury,leading to adverse cardiac remodeling.Recently published studies demonstrated that the functional repertoire of inflammatory and reparative cells may extend beyond the roles suggested by traditional teachings.This review summarizes recent advances in the cytological mechanism of the postinfarction inflammatory response in order to develop new treatment for controling inflammation to suppress pathological remodeling.

关 键 词：心肌梗死 炎症反应 细胞生物学 

分 类 号：R542.22[医药卫生—心血管疾病]