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Ubiquitin E3 Ligases and p53 in Doxorubicin-Induced Cardiotoxicity

Shingo Tachibana1, Yoichiro Otaki1, Jun Goto1

  • 1Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata 990-9585, Japan.

International Journal of Molecular Sciences
|November 13, 2025
PubMed

Insights

Doxorubicin-induced cardiotoxicity involves p53 upregulation. Ubiquitin E3 ligases regulate p53 degradation, offering potential therapeutic targets for novel cardioprotective agents against Doxorubicin-induced cardiotoxicity.

Area of Science:

  • Cardiovascular research
  • Oncology
  • Molecular biology

Background:

  • Doxorubicin (Dox) is an effective anti-cancer drug, but its use is limited by cardiotoxicity.
  • Doxorubicin-induced cardiotoxicity (DIC) causes cardiomyocyte loss via p53-mediated cell death and oxidative stress.
  • The precise mechanisms of DIC are not fully understood.

Purpose of the Study:

  • To review the role of ubiquitin E3 ligases in p53 degradation.
  • To explore the functional significance of E3 ligases in Doxorubicin-induced cardiotoxicity.
  • To highlight emerging cardioprotective agents targeting E3 ligase-mediated p53 suppression.

Main Methods:

  • Literature review focusing on recent advancements in E3 ligase research and DIC.
  • Analysis of the ubiquitin system's role in cardiovascular disease and p53 regulation.
  • Synthesis of findings on cardioprotective strategies targeting E3 ligases.

Main Results:

  • p53 plays a critical role in Doxorubicin-induced cardiotoxicity.
  • Ubiquitin E3 ligases regulate p53 degradation and are implicated in DIC.
  • Suppression of p53 in cardiomyocytes can ameliorate Doxorubicin-induced cardiotoxicity.

Conclusions:

  • Ubiquitin E3 ligases are key regulators of p53 degradation, influencing Doxorubicin-induced cardiotoxicity.
  • Targeting E3 ligase-mediated p53 suppression presents a promising therapeutic strategy for DIC.
  • Developing novel cardioprotective agents against Doxorubicin-induced cardiotoxicity is crucial.
Keywords:
Doxorubicin-induced cardiotoxicityE3 ligasep53ubiquitylation

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