Molecular pathogenetic mechanisms and new therapeutic perspectives in anthracycline-induced cardiomyopathy

Abstract

Abstract Anthracyclines are among the most powerful drugs for the treatment of oncologic diseases both in childhood and in adulthood. Nevertheless, their major antineoplastic efficacy can be seriously impaired by collateral toxic cardiac effects causing cardiomyopathy with chronic heart failure that is refractory to conventional medical therapy. This article reports possible subcellular molecular alterations of anthracycline-induced cardiomyopathy (reactive oxygen species formation, apoptosis, inflammatory signalling, altered expression of cardiomyocytes specific genes, etc) and indicates some new therapeutic perspectives resulting from a better understanding of the molecular pathogenetic mechanisms.