Role of IL-1β in Adverse Cardiac Remodeling and Heart Failure
Acute myocardial infarction (AMI) results from an abrupt oxygen supply/demand imbalance deriving from coronary atherothrombosis. Myocardial ischemia and/or ischemia-reperfusion injury determine loss of functional myocardium and induce an intense acute inflammatory response, characterized by the activation of the inflammasome and maturation of interleukin (IL)-1β and other pro-inflammatory cytokines. IL-1β induces further loss of viable myocardium, promoting cardiac dilation and dysfunction in the sub-acute phase of AMI, and suppressing cardiac contractility and β-adrenergic receptor responsiveness. Inhibitors of the inflammasome or of IL-1β given during AMI have the potential to prevent adverse cardiac remodeling and/or heart failure.