ArticleCell biology and toxicology2024
eEF2K alleviates doxorubicin-induced cardiotoxicity by inhibiting GSK3β and improving autophagy dysfunction.
Article in Cell biology and toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Dead-End protein expression, function, and mutation in cancer: a systematic review.Molecular biology reports · 2025Pooled it
- Doxorubicin-Induced Cardiotoxicity: A Comprehensive Update.Journal of cardiovascular development and disease · 2025Review
- Post-translational modifications orchestrate mTOR-driven cell death in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
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Authors and funding
15 authors.
Funding
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 microscopy in vivo, as well as LysoSensor and mRFPGFP-LC3 puncta in vitro. eEF2K overexpression improves DOX-induced autophagy blockade. In addition, eEF2K knockdown aggravated autophagy blockade and cardiomyocyte injury in DIC model. eEF2K also phosphorylated and inhibited GSK3β in DIC model. AR-A014418 (ARi), known for selectively inhibiting GSK3β, countered the effects of eEF2K knockdown, which aggravated autophagy blockade in the DIC. In conclusion, this study proposes that eEF2K alleviates DIC by inhibiting GSK3β and improving autophagy dysfunction. eEF2K is a promising therapeutic target against DIC.
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