EEF2K alleviates doxorubicin-induced cardiotoxicity by inhibiting GSK3β and improving autophagy dysfunction.

ABSTRACT: Doxorubicin-induced cardiotoxicity (DIC) poses a threat to the health and prognosis of cancer patients. It is important to find a safe and effective method for the prevention and treatment of DIC. eEF2K, which is a highly conserved α-kinase, is thought to be a therapeutic target for several human diseases. Nonetheless, it is still uncertain if eEF2K contributes to the cardiotoxic effects caused by doxorubicin (DOX). Our research revealed that eEF2K expression decreased in the DIC. eEF2K was overexpressed through adeno-associated virus in vivo and adenovirus in vitro, which presented alleviative cardiomyocyte death and cell atrophy induced by DOX. Autophagy dysfunction is one of important mechanisms in DIC. As a result, autophagic function was evaluated using Transmission electron microscop

SUBMITTER: Guan J 

PROVIDER: S-EPMC11663172 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature