Li GZ, Liu JY, Zhou H. Ferroptosis: A novel therapeutic target for diabetic cardiomyopathy. World J Diabetes 2025; 16(6): 104665 [DOI: 10.4239/wjd.v16.i6.104665]
Corresponding Author of This Article
Hong Zhou, MD, Chief Physician, Professor, Department of Endocrinology, The Second Hospital of Hebei Medical University, No. 215 Heping West Road, Shijiazhuang 050000, Hebei Province, China. zhoubs2013@hebmu.edu.cn
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. Jun 15, 2025; 16(6): 104665 Published online Jun 15, 2025. doi: 10.4239/wjd.v16.i6.104665
Ferroptosis: A novel therapeutic target for diabetic cardiomyopathy
Gui-Zhi Li, Jia-Yin Liu, Hong Zhou
Gui-Zhi Li, Hong Zhou, Department of Endocrinology, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei Province, China
Jia-Yin Liu, Department of Oncology, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, Hebei Province, China
Co-first authors: Gui-Zhi Li and Jia-Yin Liu.
Author contributions: Li GZ and Liu JY contributed equally; Li GZ contributed to conceptualization, writing - original draft; Liu JY contributed to writing - review, resources, analysis; Zhou H modified the original manuscript; All authors have read and approved the final manuscript.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Hong Zhou, MD, Chief Physician, Professor, Department of Endocrinology, The Second Hospital of Hebei Medical University, No. 215 Heping West Road, Shijiazhuang 050000, Hebei Province, China. zhoubs2013@hebmu.edu.cn
Received: December 28, 2024 Revised: March 24, 2025 Accepted: May 7, 2025 Published online: June 15, 2025 Processing time: 168 Days and 9.8 Hours
Abstract
Ferroptosis is a new type of programmed cell death caused by the accumulation of iron-dependent lipid peroxides, and it plays a role in the occurrence and progression of diverse diseases. Diabetic cardiomyopathy (DCM), a serious cardiovascular complication in patients with diabetes, eventually progresses to refractory heart failure (HF), which increases the risk of hospitalization for HF and cardiovascular death in patients with diabetes. Despite glycemic control, effective strategies to prevent DCM onset are currently lacking. Accumulating evidence suggests that ferroptosis is involved in oxidative stress, inflammation, and abnormal autophagy in diabetic myocardium, which plays an important role in myocardial apoptosis, hypertrophy, and cardiac fibrosis. The inhibition of ferroptosis can relieve DCM. Presently, ferroptosis inhibitors have been broadly suggested for the treatment of iron overload-related cardiomyopathy. This article reviewed relevant studies to offer a new therapeutic target for DCM.
Core Tip: Ferroptosis, a form of iron-dependent programmed cell death, plays a key role in the development of diabetic cardiomyopathy (DCM), contributing to oxidative stress, inflammation, and myocardial damage. Inhibiting ferroptosis can potentially alleviate DCM and prevent its progression to heart failure. This emerging pathway offers a promising therapeutic target for DCM, providing new hope for the management of DCM.
