Skip to main content

REVIEW article

Front. Physiol.
Sec. Cell Physiology
Volume 15 - 2024 | doi: 10.3389/fphys.2024.1450656
This article is part of the Research Topic Cell death programs in the pathogenesis of heart disease View all 4 articles

Role of ferroptosis in the pathogenesis of heart disease

Provisionally accepted
  • University of Washington, Seattle, United States

The final, formatted version of the article will be published soon.

    Ferroptosis is a new form of regulated necrosis characterized by iron-dependent lipid peroxidation, leading to irreparable lipid damage, membrane permeabilization, and necrotic cell death. Ferroptosis has recently been implicated in the pathogenesis of multiple forms of heart disease such as myocardial infarction, cardiac hypertrophy, heart failure, and various cardiomyopathies. Important progress has also been made regarding how ferroptosis is regulated in vitro and in vivo as well as its role in cardiac homeostasis and disease pathogenesis. In this review, we discuss molecular mechanisms that regulates ferroptosis in the heart, including pathways leading to iron overload and lipid peroxidation as well as the roles of key organelles in this process. We also discuss recent findings pertaining to the new pathogenic role of ferroptosis in various forms of heart disease as well as genetic and pharmacologic strategies targeting ferroptosis in the heart.

    Keywords: ferroptosis, Iron Overload, Lipid Peroxidation, signaling, Heart disease

    Received: 17 Jun 2024; Accepted: 30 Aug 2024.

    Copyright: © 2024 Fatima, Zhou, Chen and Liu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Qinghang Liu, University of Washington, Seattle, United States

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.