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A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
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Novel molecular mechanisms of doxorubicin cardiotoxicity: latest leading-edge advances and clinical implications

Y Robert Li1, Kassim Traore2, Hong Zhu3

  • 1Department of Pharmacology, Campbell University Jerry Wallace School of Osteopathic Medicine, Buies Creek, NC, 27560, USA. yli@campbell.edu.

Molecular and Cellular Biochemistry
|June 13, 2023
PubMed

Insights

Doxorubicin (Dox) chemotherapy causes heart damage (cardiotoxicity) through various mechanisms. Recent research highlights ferroptosis, cardiogenetics, and regulatory RNAs as key factors in Dox-induced cardiotoxicity.

Area of Science:

  • Oncology
  • Cardiology
  • Molecular Biology

Background:

  • Doxorubicin (Dox) is a vital chemotherapy drug, but its use is restricted by cardiotoxicity.
  • Established mechanisms of Dox-induced cardiotoxicity (DIC) include oxidative stress, topoisomerase inhibition, and mitochondrial damage.

Purpose of the Study:

  • To review recent advances in understanding the molecular mechanisms of Dox-induced cardiotoxicity.
  • To focus on cutting-edge discoveries in influential journals.

Main Methods:

  • Literature review of recent mechanistic studies on Dox-induced cardiotoxicity.
  • Focus on novel molecular targets and signaling pathways.

Main Results:

  • Ferroptosis identified as a significant form of cell death in Dox cytotoxicity.
  • Elucidation of the roles of cardiogenetics and regulatory RNAs in DIC.
  • Identification of multiple other novel targets and pathways.

Conclusions:

  • Recent research has significantly advanced the understanding of Dox-induced cardiotoxicity mechanisms.
  • Emerging areas like ferroptosis, cardiogenetics, and regulatory RNAs offer new therapeutic targets for mitigating DIC.
Keywords:
CardiogeneticsCardiomyopathyCardiotoxicityDoxorubicinFerroptosisHemeHemopexinMacrophageMitochondriaNrf1Regulatory RNA

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