炎症反应在心梗后心衰发病过程中的作用研究进展

心梗后心衰是慢性心力衰竭中最常见的类型，近年研究发现炎症反应迅速、持续的激活是心梗后心衰的重要特征。适当的炎症反应可以减少心肌梗死范围，促进瘢痕形成及缺血心肌的恢复，而炎症反应过度、持久激活可促进心脏扩大、心功能不全及心力衰竭。心肌梗死后心肌细胞释放坏死物质，通过激活 TLR 介导的通路、补体系统以及 ROS 诱导的通路调控 NF-κB 相关通路，激活体内固有免疫。同时中性粒细胞、单核细胞、巨噬细胞等多种细胞参与了炎症过程。如何通过调控心梗后心衰过程中的炎症反应从而抑制病理性重构为心衰的治疗提供了新的方向。本文从炎症反应激活过程中的细胞基础及相关通路两方面，对炎症反应在心梗后心衰过程中的作用及机制做一系统综述，为进一步研究心衰过程中炎症反应的作用及抗炎治疗提供参考。 

Progress in effects and regulation of inflammatory response in post-infarction heart failure

Myocardial infarction is the most common cause that induces heart failure. Recent studies have identified that instant and prolonged activation of inflammatory response is a key character of post-infarction heart failure. Inflammatory response to some degree can promote wound healing, scar formation and recovery of ischemic myocardium, but excessive inflammation could play an important role in the development of chamber dilation, systolic dysfunction and heart failure. Extensive necrosis in the infarcted myocardium triggers the innate immune response through stimulating Toll-Like Receptor (TLR) mediated signaling, activating the complement cascade and reactive oxygen species (ROS) pathway, and regulating the Nuclear Factor (NF)- κB system. Neutrophils, mononuclear cells, macrophages and other kinds of cells play essential roles in inf lammation. How to control inflammation to suppress pathological remodeling is an important issue to be considered in developing new treatment for heart failure. This review summarizes the roles of related cells and signal pathways in the pathophysiological mechanisms of inflammation in myocardial induced heart failure in order to provide references for further study in the effects of inflammation and anti-inflammatory therapies in heart failure.