Exploring Anthracycline-Induced Cardiotoxicity from the Perspective of Protein Quality Control.

Area of Science:

• Cardiology
• Oncology
• Molecular Biology

Background:

• Anthracyclines are vital anticancer agents but induce dose-dependent myocardial toxicity, restricting their clinical use.
• The precise mechanisms underlying anthracycline cardiotoxicity remain incompletely understood.
• Cardiomyocytes' terminally differentiated nature necessitates robust protein quality control for cardiac stability.

Purpose of the Study:

• To review the current understanding of anthracycline-induced cardiotoxicity.
• To highlight the role of protein quality control pathways, specifically autophagy and the ubiquitin-proteasome system, in mitigating this toxicity.
• To provide a theoretical basis for managing anthracycline therapy.

Main Methods:

• Literature review of studies on anthracycline cardiotoxicity.
• Analysis of research on protein quality control mechanisms (autophagy and ubiquitin-proteasome system).
• Integration of findings to connect protein quality control to anthracycline-induced cardiac damage.

Main Results:

• Protein quality control mechanisms are essential for maintaining cardiomyocyte health.
• Dysregulation of autophagy and the ubiquitin-proteasome system contributes to anthracycline cardiotoxicity.
• Further research into metabolic pathways governing protein quality control is warranted.

Conclusions:

• Protein quality control pathways are critical in the context of anthracycline cardiotoxicity.
• Targeting these pathways may offer novel strategies for preventing or treating anthracycline-induced heart damage.
• This review supports clinicians in the application and management of anthracyclines.