Figure 2.

Overview of the inflammatory response to acute myocardial infarction. The figure outlines the pro-inflammatory and anti-inflammatory phases after MI. Myocardial ischemia leads to cell necrosis after MI. Necrotic cardiomyocytes induce inflammation by producing complement, ROS, and DAMPS. Complement induces the aggregation of cells, such as neutrophils, B lymphocytes, and macrophages, to the infarcted myocardium by releasing related cytokines. A variety of DAMPS can be produced by cardiac resident necrotic cells after myocardial infarction. DAMPS can bind to Toll-like receptors on endothelial cells and cardiomyocytes, promote ROS production by endothelial cells, and also cause cardiomyocyte necrosis and activate leukocytes. In addition, DAMPS are able to stimulate the release of inflammatory cytokines and chemokines from fibroblasts. In the anti-inflammatory stage, monocytes, neutrophils, and macrophages will undergo changes and work with Tregs, MDSC, and dendritic cells to secrete anti-inflammatory cytokines to resolve the inflammatory response, so that the damaged heart will enter the next repair stage. This figure was drawn using figdraw (https://www.figdraw.com, accessed on 20 March 2024), export ID: RUAOP72570.