Authors
Giulia Guerra, Francesco Niro, Marco Mergiotti, Giovanni Gavatorta, Emilio Hirsch, Alessandra Ghigo
Published in
British journal of pharmacology. Sep 07, 2026. Epub Sep 07, 2026.
Abstract
Anthracyclines remain a cornerstone of anticancer therapy, but their clinical use is limited by cancer therapy-related cardiac dysfunction, a major contributor to long-term cardiovascular morbidity in cancer survivors. Although traditionally attributed to oxidative stress, DNA damage and mitochondrial toxicity, emerging evidence identifies disruption of metabolism as a central mechanism of anthracycline-induced cardiotoxicity. Anthracycline exposure promotes a distinct metabolic phenotype characterized by impaired mitochondrial oxidative phosphorylation, dysregulated metabolism of fatty acids and glucose, along with decreased metabolic flexibility, ultimately resulting in inefficient myocardial energetics. These changes are modulated by the patient's underlying cardiometabolic status, suggesting that metabolic reserve influences susceptibility to injury. In addition to direct myocardial effects, anthracyclines induce systemic metabolic changes that affect substrate availability and inter-organ communication. This review focuses on cardiotoxicity induced by anthracyclines, particularly by doxorubicin, highlighting mitochondrial dysfunction, altered substrate utilization and metabolic inflexibility in comparison with other cardiac diseases. We also discuss the newly emerging metabolic strategies aimed at improving cardioprotection.
PMID:
42706774
Bibliographic data and abstract were imported from PubMed on 08 Sep 2026.
Read full publication at:
Please sign in
to see all details.
Advertisement
Stats
- Recommendations n/a n/a positive of 0 vote(s)
- Views 7
- Comments 0