Doxorubicin‑induced cardiomyopathy is mitigated by empagliflozin via the modulation of endoplasmic reticulum stress pathways

Abstract

doxorubicin (dox) exhibits a high efficacy in the treatment of numerous types of cancer. However, the beneficial cytotoxic effects of dox are often accompanied by an increase in the risk of cardiotoxicity. oxidative stress (oS) plays a key role in dox‑induced cardiomyopathy (dic). oS in cardiomyocytes disrupts endoplasmic reticulum (er) function, leading to the accumulation of misfolded/unfolded proteins known as er stress. er stress acts as an adaptive mechanism; however, prolonged er stress together with oS may lead to the initiation of cardiomyocyte apoptosis. The present study aimed to explore the potential of an anti‑diabetic drug, empagliflozin (EMPA), in mitigating Dox‑induced ER stress and cardiomyocyte apoptosis. in the present study, the effects of 1 h pretreatment of eMPa on dox‑treated cardiomyocytes isolated from Sprague‑dawley rats were investigated. after 24 h, eMPa pre‑treatment promoted cell