Exploring Anthracycline-Induced Cardiotoxicity from the Perspective of Protein Quality Control
Shanshan Li, Weihua Niu, Chunyan Wang, Jie Zhao, Na Zhang, Yue Yin, Mei Jia, Liyan Cui
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.
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…
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Taxonomy
TopicsChemotherapy-induced cardiotoxicity and mitigation · Endoplasmic Reticulum Stress and Disease · Autophagy in Disease and Therapy