Zooming in and out of ferroptosis in human disease.
10.1007/s11684-023-0992-z
- Author:
Xue WANG
1
;
Ye ZHOU
2
;
Junxia MIN
3
;
Fudi WANG
4
Author Information
1. The Second Affiliated Hospital, The First Affiliated Hospital, Institute of Translational Medicine, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine, Hangzhou, 310058, China.
2. Department of Endocrinology and Metabolism, Ningbo First Hospital, Ningbo, 315000, China.
3. The Second Affiliated Hospital, The First Affiliated Hospital, Institute of Translational Medicine, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine, Hangzhou, 310058, China. junxiamin@zju.edu.cn.
4. The Second Affiliated Hospital, The First Affiliated Hospital, Institute of Translational Medicine, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine, Hangzhou, 310058, China. fwang@zju.edu.cn.
- Publication Type:Review
- Keywords:
antioxidation;
ferroptosis;
human disease;
iron metabolism;
lipid peroxidation
- MeSH:
Humans;
Ferroptosis;
Autoimmune Diseases;
Cardiovascular Diseases;
Iron;
Musculoskeletal Diseases
- From:
Frontiers of Medicine
2023;17(2):173-206
- CountryChina
- Language:English
-
Abstract:
Ferroptosis is defined as an iron-dependent regulated form of cell death driven by lipid peroxidation. In the past decade, it has been implicated in the pathogenesis of various diseases that together involve almost every organ of the body, including various cancers, neurodegenerative diseases, cardiovascular diseases, lung diseases, liver diseases, kidney diseases, endocrine metabolic diseases, iron-overload-related diseases, orthopedic diseases and autoimmune diseases. Understanding the underlying molecular mechanisms of ferroptosis and its regulatory pathways could provide additional strategies for the management of these disease conditions. Indeed, there are an expanding number of studies suggesting that ferroptosis serves as a bona-fide target for the prevention and treatment of these diseases in relevant pre-clinical models. In this review, we summarize the progress in the research into ferroptosis and its regulatory mechanisms in human disease, while providing evidence in support of ferroptosis as a target for the treatment of these diseases. We also discuss our perspectives on the future directions in the targeting of ferroptosis in human disease.
