Review reveals multi-pathway drivers of anthracycline cardiotoxicity in oncology models, highlighting potential targets for cardioprotective therapy.
Key Points
Anthracycline antineoplastic therapy triggers severe cardiotoxicity through cardiomyocyte dysfunction and pathological death, which restricts therapeutic dosing.
Cardiac injury involves mitochondrial dysfunction, topoisomerase inhibition, disrupted iron metabolism, and oxidative stress alongside transport pathway uptake.
Review of animal experiments and human induced pluripotent stem cell models reveals novel cardioprotective mechanisms to mitigate doxorubicin toxicity in cancer.