Ferroptosis, a therapeutic target - Review - The initiation, progression, and therapeutic management of ferroptosis in disease

Sep 21, 2026

The identification of ferroptosis represents a pivotal advancement in cell death research, revealing a novel mechanism underlying cellular demise and informing how ferroptosis is initiated, progresses, and can be therapeutically managed. Ferroptosis is primarily driven by intracellular iron accumulation, lipid peroxidation, or defects in antioxidant defense, leading to membrane rupture and cell death. Evidence links ferroptosis to diverse diseases, and understanding its mechanisms supports development of innovative treatment strategies and improved patient outcomes.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages25

Reading Time1 h 3 min

AccessFree to download

Abstract

Introduction

Ferroptosis as a programmed cell death mechanism

Links to cardiovascular diseases

Links to neurodegenerative diseases

Links to cancer and treatment context

Li et al. Journal of Translational Medicine (2024) 22:1137 [https://doi.org/10.1186/s12967-024-05881-6](https://doi.org/10.1186/s12967-024-05881-6) Journal of Translational Medicine REVIEW Open Access Ferroptosis, a therapeutic target for cardiovascular diseases, neurodegenerative diseases and cancer Yinghui Li 1†, Cuiyun Liu1†, Bo Fang1†, Xinzhe Chen1, Kai Wang1, Hui Xin2*, Kun Wang1* and Su-Min Yang1* Abstract The identification of ferroptosis represents a pivotal advancement in the field of cell death research, revealing an entirely novel mechanism of cellular demise and offering new insights into the initiation, progression, and therapeutic management of various diseases. Ferroptosis is predominantly induced by intracellular iron accumulation, lipid peroxidation, or impairments in the antioxidant defense system, culminating in membrane rupture and consequent cell death. Studies have associated ferroptosis with a wide range of diseases, and by enhancing our comprehension of its underlying mechanisms, we can formulate innovative therapeutic strategies, thereby providing renewed hope for patients. Keywords Ferroptosis, Cardiovascular diseases, Neurodegenerative diseases, Cancer, Immunotherapy Introduction In 2012, the concept of ferroptosis—a unique kind of programmed cell death—was put forth. It is characterized by aberrant iron metabolism, excessive accumulation of reactive oxygen species (ROS), and lipid peroxides that are dependent on iron [1]. Ferroptosis has recently gained attention in biomedical research, and emergent research elucidates the pivotal role ferroptosis assumes in myriad physiological and pathological episodes, including cardiovascular diseases (CVDs), neurodegenerative †Yinghui Li, Cuiyun Liu, and Bo Fang are Co-author. *Correspondence: Hui Xin huixin20241 [1@163.com](1@163.com) Kun Wang [wangk696@qdu.edu.cn](wangk696@qdu.edu.cn)[ ](wangk696@qdu.edu.cn)Su-Min Yang [ysumin2024@126.com](ysumin2024@126.com) 1 Department of Cardiovascular Surgery, The Affiliated Hospital of Qingdao University, College of Medicine, Qingdao University, Qingdao 266021, China 2 Department of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao 266021, China diseases (NDs) and cancer. In these three disease types, oxidative stress and inflammation are critical factors that can lead to ferroptosis, which may interact with and exacerbate disease progression. Particularly during cancer treatment, chemotherapy and radiation can contribute to CVDs and NDs. Thus, ferroptosis could be a shared pathological mechanism among these conditions, and targeting it may present a new therapeutic approach [2, 3]. Inhibiting iron ion aggregation, using antioxidants, and ferritin autophagy are the main goals of current treatment approaches to ferroptosis [4, 5]. For clinical use, further research and inquiry are still required, despite certain studies demonstrating the promise of various treatment approaches. Although research on ferroptosis in CVDs is still in its infancy, there is mounting evidence that it plays a part in their development and progression. At present, the intricate relationship between ferroptosis and CVDs is mainly focused on cardiac ischemia–reperfusion, atherosclerosis, and heart failure [6, 7] . Myocardial cells are harmed by hypoxia and ischemia during myocardial infarction, which causes an imbalance in © The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party

FAQs

What mechanism defines ferroptosis?

Ferroptosis is characterized by iron-dependent lipid peroxidation and impaired antioxidant defenses, driven by abnormal iron metabolism and reactive oxygen species accumulation, ultimately causing membrane rupture and cell death.

Why is ferroptosis considered relevant to cardiovascular diseases?

In cardiovascular conditions such as cardiac ischemia–reperfusion, atherosclerosis, and heart failure, oxidative stress and inflammation contribute to ferroptosis, which may interact with and exacerbate disease progression.

How might ferroptosis be targeted for therapeutic benefit?

Current approaches focus on inhibiting iron ion aggregation, using antioxidants, and leveraging ferritin autophagy; further research is needed to translate these strategies into clinical use.

Sep 21, 2026

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