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Ferroptosis in Myocardial Fibrosis: Mechanisms and Therapeutic Insights

Xuefeng Lin1, Weijun Li1, Jiahao Ye1

  • 1College of Chinese Medicine, Hunan University of Chinese Medicine, Changsha 410208, China.

Antioxidants (Basel, Switzerland)
|January 28, 2026
PubMed

Insights

Ferroptosis, a cell death process, is increasingly linked to myocardial fibrosis (MF). Targeting ferroptosis mechanisms offers a novel therapeutic strategy for treating cardiac dysfunction and MF.

Area of Science:

  • Cardiovascular Research
  • Cell Death Mechanisms
  • Biomedical Science

Background:

  • Myocardial fibrosis (MF) is a pathological hallmark of cardiac disorders, driven by extracellular matrix deposition and fibroblast activation.
  • The precise molecular mechanisms underlying MF progression remain largely unknown.
  • Ferroptosis, a regulated cell death pathway involving iron and lipid peroxidation, is emerging as a significant factor in MF.

Purpose of the Study:

  • To systematically review the intricate mechanisms linking ferroptosis to myocardial fibrosis.
  • To explore ferroptosis's role in MF pathogenesis from multiple molecular dimensions.
  • To offer novel perspectives for understanding and treating MF.

Main Methods:

  • Comprehensive literature search of PubMed and Web of Science databases.
  • Focus on studies published from 2020 to July 2025.
  • Systematic analysis and review of ferroptosis mechanisms in MF.

Main Results:

  • Ferroptosis is implicated in the onset and advancement of myocardial fibrosis.
  • Disruptions in iron metabolism, lipid peroxidation, and glutathione balance are key contributors.
  • Dysregulated ferroptosis pathways are central to MF development.

Conclusions:

  • Modulating ferroptosis presents a promising therapeutic avenue for myocardial fibrosis.
  • Understanding ferroptosis mechanisms is crucial for developing targeted MF treatments.
  • This review provides innovative insights into MF molecular mechanisms and potential therapies.
Keywords:
Nrf2 signaling pathwayferroptosisglutathione metabolismlipid peroxidationmyocardial fibrosis

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