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

## TL;DR

This paper reviews how protein quality control mechanisms may be linked to heart damage caused by anthracycline chemotherapy drugs.

## Contribution

The paper highlights the role of autophagy and the ubiquitin-proteasome system in anthracycline-induced cardiotoxicity.

## Key findings

- Anthracyclines cause irreversible heart damage, but the mechanism is not fully understood.
- Protein quality control systems like autophagy and the ubiquitin-proteasome system are crucial for heart cell health.
- Understanding these systems could improve the clinical use and management of anthracyclines.

## Abstract

Anthracyclines are effective anticancer drugs; however, their use is restricted
because of their dose-dependent, time-dependent and irreversible myocardial
toxicity. The mechanism of anthracycline cardiotoxicity has been widely studied
but remains unclear. Protein quality control is crucial to the stability of the
intracellular environment and, ultimately, to the heart because cardiomyocytes
are terminally differentiated. Two evolutionarily conserved mechanisms,
autophagy, and the ubiquitin-proteasome system, synergistically degrade misfolded
proteins and remove defective organelles. Recent studies demonstrated the
importance of these mechanisms. Further studies will reveal the detailed
metabolic pathway and metabolic control of the protein quality control mechanism
integrated into anthracycline-induced cardiotoxicity. This review provides
theoretical support for clinicians in the application and management of
anthracyclines.