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Understanding Anthracycline Cardiotoxicity From Mitochondrial Aspect.

Junqi Huang1, Rundong Wu2, Linyi Chen2

  • 1Key Laboratory for Regenerative Medicine, Ministry of Education, College of Life Science and Technology, Jinan University, Guangzhou, China.

Frontiers in Pharmacology
|February 25, 2022
PubMed
Summary

Anthracyclines cause heart damage by affecting mitochondria. This review explores how mitochondria, reactive oxygen species, iron overload, and metabolism changes contribute to this cardiotoxicity.

Keywords:
ROSanthracyclinecardiotoxicityferroptosismetabolismmitochondriamitophagy

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Area of Science:

  • Cardiology
  • Oncology
  • Mitochondrial Biology

Background:

  • Anthracyclines are vital chemotherapy agents for various cancers.
  • Anthracycline-induced cardiotoxicity limits their clinical application.
  • The precise mechanisms of anthracycline cardiotoxicity are not fully understood.

Purpose of the Study:

  • To review current research on the mitochondrial mechanisms of anthracycline cardiotoxicity.
  • To highlight the role of mitochondria as a primary target of anthracyclines in the heart.
  • To discuss key pathways involved in anthracycline-induced cardiac dysfunction.

Main Methods:

  • Literature review of recent findings on anthracycline cardiotoxicity.
  • Focus on mitochondrial mechanisms including ROS production, iron overload, and ferroptosis.
  • Analysis of autophagy, mitophagy, mitochondrial dynamics, and cardiac metabolism.

Main Results:

  • Mitochondria are central to anthracycline cardiotoxicity, producing reactive oxygen species (ROS) that damage mitochondria.
  • Mitochondrial iron overload and subsequent ferroptosis are implicated in cardiac injury.
  • Disruptions in autophagy, mitophagy, mitochondrial dynamics, and cardiac metabolism contribute to cardiotoxicity.

Conclusions:

  • Mitochondrial dysfunction is a key driver of anthracycline cardiotoxicity.
  • Understanding these mechanisms may lead to strategies to mitigate cardiac side effects.
  • Further research into mitochondrial pathways is crucial for safer cancer chemotherapy.