The role of ferroptosis in doxorubicin-induced cardiotoxicity – An update

Doxorubicin is a chemotherapeutic drug used in the treatment of a variety of cancers, such as cancer of the blood, bladder, breast, lymph system, stomach, neuroblasts, etc. Currently, its potential is severely limited as it leads to cardiotoxicity, a fatal side effect. Several studies have been carried out in the past few decades to elucidate the molecular mechanisms of this Doxorubicin-induced cardiotoxicity. This study aims to analyse the role of ferroptosis in the mechanism of Doxorubicin-induced cardiotoxicity, an area which remains comparatively unexplored. The article elaborates on the molecular pathogenesis of ferroptosis and the role of doxorubicin in triggering the same. Several biological pathways, especially Nrf2 (Nuclear factor erythroid 2-related factor 2)-mediated pathways, are influenced by doxorubicin, leading to ferroptosis. The study of molecular mechanisms of doxorubicin-induced cardiotoxicity is instrumental for developing therapeutic interventions that alleviate cardiotoxicity and improve the outcomes of doxorubicin usage, such as targeting ferritinophagy, which is one of the key factors in causing ferroptosis, and can reduce cardiotoxicity and can be a potential therapeutic strategy.