Lung remodeling and pulmonary hypertension after myocardial infarction: pathogenic role of reduced caveolin expression

Abstract

Thus, down-modulation of pulmonary Cav-1 and Cav-2 expression in rats subjected to MI may represent an initiating mechanism leading to the activation of the STAT3/Cyclins pathway and, ultimately, to the development of PH and lung structural remodeling.