炎症反应在心梗后心衰发病过程中的作用研究进展

Myocardial infarction is the most common cause that induces heart failure. Recent studies have identified thatinstant and prolonged activation of inflammatory response is a key character of post-infarction heart failure. Inflammatoryresponse to some degree can promote wound healing, scar formation and recovery of ischemic myocardium, but excessiveinflammation 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 theNuclear Factor (NF)- B system. Neutrophils, mononuclear cells, macrophages and other kinds of cells play essential roles ininflammation. How to control inflammation to suppress pathological remodeling is an important issue to be considered indeveloping new treatment for heart failure. This review summarizes the roles of related cells and signal pathways in thepathophysiological mechanisms of inflammation in myocardial induced heart failure in order to provide references for furtherstudy in the effects of inflammation and anti-inflammatory therapies in heart failure.