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Role of Ferroptosis in Stroke
Yunfei Xu1,2,3,4, Kexin Li1,2,3,4, Yao Zhao1,2,3,4
1Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Insights
Ferroptosis, an iron-dependent cell death, is implicated in stroke pathogenesis. Targeting ferroptosis pathways shows promise for novel stroke treatments by modulating lipid peroxidation and iron metabolism.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Stroke is a leading cause of death and disability worldwide, stemming from cardiovascular events like rupture or blockage.
- Risk factors include hypertension, hyperlipidemia, hyperglycemia, smoking, and advanced age, leading to hemorrhagic or ischemic stroke.
- Ferroptosis, a novel iron-dependent cell death marked by lipid peroxidation, is increasingly recognized in various diseases.
Purpose of the Study:
- To systematically review the role of ferroptosis in stroke pathogenesis.
- To explore the therapeutic potential of targeting ferroptosis for stroke treatment.
Main Methods:
- Literature review and synthesis of existing research on ferroptosis and stroke.
- Analysis of molecular mechanisms linking iron metabolism, lipid peroxidation, and cell death in stroke models.
Main Results:
- Stroke induces iron overload and lipid metabolism dysfunction, promoting ferroptosis.
- The glutathione (GSH)/glutathione peroxidase 4 (GPX4) pathway and antioxidants like Coenzyme Q10 (CoQ10), Ferrostatin-1 (Fer-1), and Liproxstatin-1 (Lip-1) can inhibit ferroptosis.
- Intervention in ferroptosis pathways has shown success in animal stroke models.
Conclusions:
- Ferroptosis is a significant contributor to stroke pathology.
- Modulating ferroptosis presents a promising therapeutic strategy for stroke management.
Abstract:
Stroke is a common and serious nervous system disease caused by the rupture or blockage of the cardiovascular system. It causes millions of deaths and disabilities every year, which is a huge burden on humanity. It may be induced by thrombosis, hypertension, hyperlipidemia, hyperglycemia, smoking, advanced age and so on. According to different causes, stroke can be generally divided into hemorrhagic stroke and ischemic stroke, whose pathogenesis and treatment are quite different. Ferroptosis is a new type of cell death first defined in 2012, which is characterized by non-apoptotic, iron-dependent, and over-accumulated lipid peroxides. Excess lipid reactive oxygen species produced during ferroptosis eventually leads to oxidative cell death. Ferroptosis has been shown to occur and play an important role in tumors, neurological diseases, kidney injury, and ischemia-reperfusion injury. Ferroptosis is also closely related to the pathogenesis of stroke. Moreover, scientists have successfully intervened in the process of stroke in animal models by regulating ferroptosis, indicating that ferroptosis is a new potential target for the treatment of stroke. This paper systematically summarizes the involvement and role of ferroptosis in the pathogenesis of stroke and predicts the potential of ferroptosis in the treatment of stroke. Ferroptosis in stroke. Stroke induces iron overload and lipid metabolism disorders. Elevated iron catalyzes lipid peroxidation and eventually triggers ferroptosis. Conversely, the GSH/GPX4 pathway, as well as CoQ10, Fer-1, and Lip-1, inhibits lipid peroxidation and, thus, alleviates ferroptosis. GSH glutathione; GPX4 glutathione peroxidase 4; CoQ10 coenzyme Q10; Lip-1 liproxstatin-1; Fer-1 ferostatin-1.
