Ferroptosis Mediated by Lipid Reactive Oxygen Species: A Possible Causal Link of Neuroinflammation to Neurological Disorders.
Ying ChengYiting SongHuan ChenQianqian LiYuan GaoGuanchao LuChengliang LuoPublished in: Oxidative medicine and cellular longevity (2021)
Increasing evidence indicates a possible causal link between neuroinflammation and neurological disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and stroke. A putative mechanism underlying such a link can be explained by ferroptosis. Current studies have shown that disturbances of iron homeostasis, glutamate excitatory toxicity, lipid reactive oxygen species (ROS), and other manifestations related to ferroptosis can be detected in several neurological disorders caused by neuroinflammation. To date, compelling evidence indicates that damage-associated molecular pattern (DAMP) molecules (e.g., ROS) produced in the process of ferroptosis activate glial cells by activating neuroimmune pathways and then produce a series of inflammatory factors which contribute to neurological disorders. Our review article provides a current view of the involvement of ferroptosis or ROS in the pathological process of neuroinflammation, the effects of neuroinflammation mediated by ferroptosis in neurological disorders, a better understanding of the mechanisms underlying ferroptosis participates in neuroinflammation, and the potential treatments for neurological disorders. In addition, further research on the mechanisms of ferroptosis as well as the link between ferroptosis and neuroinflammation will help provide new targets for treatment.
Keyphrases
- cell death
- cerebral ischemia
- reactive oxygen species
- cell cycle arrest
- lipopolysaccharide induced
- traumatic brain injury
- lps induced
- cognitive impairment
- subarachnoid hemorrhage
- oxidative stress
- blood brain barrier
- brain injury
- signaling pathway
- cell proliferation
- atrial fibrillation
- single molecule
- spinal cord injury
- replacement therapy
- human health
- fatty acid
- case control
- drug induced
- oxide nanoparticles