Alteration of the monocyte repertoire after myocardial infarction – novel mechanistic insights and therapeutic avenues
Myocardial infarction (MI) is a major contributor to worldwide morbidity and mortality. MI occurs after atherosclerotic plaque rupture/erosion leading to atherothrombosis which in turn blocks supply of oxygenated blood to areas of the heart. Consequently, parts of the heart muscle become hypoxic and die off. This triggers a systemic inflammatory reaction which leads to an accumulation of inflammatory cells in the infarct area. These blood-derived immune cells exert different function during the course of MI.