GPX4, ferroptosis, and diseases

GPX4 (Glutathione peroxidase 4) serves as a crucial intracellular regulatory factor, participating in various physiological processes and playing a significant role in maintaining the redox homeostasis within the body. Ferroptosis, a form of iron-dependent non-apoptotic cell death, has gained consid...

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Published in:Biomedicine & pharmacotherapy 2024-05, Vol.174, p.116512-116512, Article 116512
Main Authors: Zhang, Wangzheqi, Liu, Yang, Liao, Yan, Zhu, Chenglong, Zou, Zui
Format: Article
Language:English
Subjects:
Animals
Cancer
Cardiovascular diseases
Ferroptosis
Ferroptosis - physiology
GPX4
Humans
Ischemia reperfusion injury
Neoplasms - metabolism
Neoplasms - pathology
Nervous system diseases
Phospholipid Hydroperoxide Glutathione Peroxidase - metabolism
Sepsis
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Summary:GPX4 (Glutathione peroxidase 4) serves as a crucial intracellular regulatory factor, participating in various physiological processes and playing a significant role in maintaining the redox homeostasis within the body. Ferroptosis, a form of iron-dependent non-apoptotic cell death, has gained considerable attention in recent years due to its involvement in multiple pathological processes. GPX4 is closely associated with ferroptosis and functions as the primary inhibitor of this process. Together, GPX4 and ferroptosis contribute to the pathophysiology of several diseases, including sepsis, nervous system diseases, ischemia reperfusion injury, cardiovascular diseases, and cancer. This review comprehensively explores the regulatory roles and impacts of GPX4 and ferroptosis in the development and progression of these diseases, with the aim of providing insights for identifying potential therapeutic strategies in the future. [Display omitted] •GPX4, as a crucial antagonist of ferroptosis, is intimately associated with multiple diseases.•The prospect of targeting GPX4 for the treatment of diseases related to ferroptosis is profoundly promising.•GPX4 as a key target to counteract ferroptosis is closely related to diseases.
ISSN:0753-3322
1950-6007
DOI:10.1016/j.biopha.2024.116512