Fig. 3.

Coronary artery occlusion, myocardial infarction, and prolonged ischemia result in an intense post-MI inflammatory response. In the setting of ischemia, cardiomyocytes lose their ability to contract to drive blood flow. Instead, these cells become necrotic, releasing DAMPs and pro-inflammatory cytokines into their interstitial environment. This attracts neutrophils, and macrophages follow, to the site of infarction. Infiltrating immune cells secrete MMPs that degrade the existing ECM to pave a path for immune cells to remove necrotic cardiomyocytes and ECM debris as inflammation persists