Abstract
Cardiovascular disease (CVD) is one of the leading causes of death worldwide. One of the most common implications of CVD is myocardial infarction (MI). Following MI, the repair of the infarcted heart occurs through three distinct, yet overlapping phases of inflammation, proliferation, and maturation. Macrophages are essential to the resolution of the inflammatory phase due to their role in phagocytosis and efferocytosis. However, excessive and long-term macrophage accumulation at the area of injury and dysregulated function can induce adverse cardiac remodeling post-MI. Ubiquitin (UB) is a highly evolutionarily conserved small protein and is a normal constituent of plasma. Levels of UB are increased in the plasma during a variety of pathological conditions, including ischemic heart disease. Treatment of mice with UB associates with decreased inflammatory response and improved heart function following ischemia/reperfusion injury. This review summarizes the role of macrophages in the infarct healing process of the heart post-MI, and discusses the role of exogenous UB in myocardial remodeling post-MI and in the modulation of macrophage phenotype and function.