# Ferroptosis in Myocardial Fibrosis: Mechanisms and Therapeutic Insights

## TL;DR

This paper explores how ferroptosis, a type of cell death, contributes to heart tissue scarring and suggests it as a potential target for new treatments.

## Contribution

The paper systematically reviews the mechanisms linking ferroptosis to myocardial fibrosis and highlights therapeutic opportunities.

## Key findings

- Ferroptosis is closely associated with the progression of myocardial fibrosis.
- Iron metabolism, lipid peroxidation, and glutathione imbalance are key factors in this process.
- Targeting ferroptosis pathways offers a novel therapeutic strategy for treating cardiac fibrosis.

## Abstract

Myocardial fibrosis (MF) is a common pathological feature of diverse cardiac disorders and is a key driving factor of cardiac dysfunction. It is marked by excessive deposition of extracellular matrix (ECM) proteins, particularly collagen type I and III, and a prolonged activation of cardiac fibroblasts. However, the molecular drivers of this process remain undetermined. Ferroptosis is an iron-catalyzed, lipid-peroxidation-dependent mode of regulated cell death. Research indicates that ferroptosis is significantly involved in the onset and advancement of MF; consequently, developing therapies that selectively modulate ferroptosis presents a promising direction of treatment options. Therefore, this paper systematically discusses the mechanisms associated with ferroptosis to explore the link between ferroptosis and MF from multiple dimensions, including iron metabolism disorders, lipid peroxidation, imbalance of glutathione metabolism, and the dysregulated activation of ferroptosis regulatory pathways, to provide innovative perspectives for the study of the specific molecular mechanisms and treatment of MF. Method: By retrieving the literature on the mechanism of ferroptosis in MF published in PubMed and Web of Science databases from 2020 to July 2025, the mechanism of action was systematically analyzed and reviewed.