Abstract

Inhibition of the blood fibrinolytic system (plasminogen/plasmin) occurs either at the level of plasminogen activators, regulated by specific plasminogen activator inhibitors (PAIs) or at the level of plasmin, mainly regulated by α2-antiplasmin (α2-AP). In this contribution, we focused on the roles of α2-AP in acute myocardial infarction and vascular remodeling associated with cardiovascular diseases. Our findings have identified a new target for the development of new therapeutics for the clinical therapy of cardiovascular diseases.

Keywords: antiplasmin, myocardial infarction, re-endothelialization, vegf, vegfr-1