The role of polyunsaturated fatty acid lipid peroxidation in ferroptosis after intracerebral hemorrhage: a review of mecha-nisms and therapeutic implications.
10.3724/zdxbyxb-2025-0329
- Author:
Man GUO
1
,
2
;
Guohui ZHAO
3
;
Zhibiao CAI
4
;
Zhenyu ZHANG
3
;
Jie ZHOU
2
,
5
Author Information
1. First Clinical Medical College, Gansu University of Chinese Medicine, Lanzhou 730000, China. gm1614038615@
2. com.
3. First Clinical Medical College, Gansu University of Chinese Medicine, Lanzhou 730000, China.
4. Depart-ment of Neurosurgery, the 940th Hospital of Joint Logistics Support Force of Chinese People's Liberation Army, Lanzhou 730050, China.
5. Depart-ment of Neurosurgery, the 940th Hospital of Joint Logistics Support Force of Chinese People's Liberation Army, Lanzhou 730050, China. zhoujie133331@
- Publication Type:English Abstract
- Keywords:
Ferroptosis;
Intracerebral hemorrhage;
Lipid peroxidation;
Polyunsaturated fatty acid;
Review
- MeSH:
Ferroptosis/physiology*;
Humans;
Cerebral Hemorrhage/pathology*;
Lipid Peroxidation;
Fatty Acids, Unsaturated/metabolism*;
Reactive Oxygen Species/metabolism*;
Iron/metabolism*;
Animals;
Mitochondria/metabolism*
- From:
Journal of Zhejiang University. Medical sciences
2025;54(5):694-704
- CountryChina
- Language:Chinese
-
Abstract:
Ferroptosis, a regulated cell death process distinct from apoptosis, is characterized by iron dysregulation and reactive oxygen species (ROS) accumulation. After intracerebral hemorrhage (ICH), decreased cerebral blood flow and iron released from erythrocytes trigger lipid peroxidation-particularly of polyunsaturated fatty acids (PUFAs)-through a cascade of reactions in local brain tissues, promoting ferroptosis. Mitochondrial dysfunction and neuroinflammation further elevate ROS, exacerbating lipid peroxidation and accelerating neuronal ferroptosis. Thus, PUFA peroxidation and associated metabolic pathways play a critical role in ICH-related neuronal damage. This review summarizes current understanding of how PUFA peroxidation contributes to ferro-ptosis after ICH, discusses key regulatory mechanisms involving lipid and iron metabolism, and highlights potential therapeutic strategies targeting ferroptosis to improve neurological outcomes.