Mechanism of Ferroptosis and Its Relationships with Other Types of Programmed Cell Death: Insights for Potential Therapeutic Benefits in Traumatic Brain Injury.
Qiuyu PangLexin ZhengZhiyang RenHeng XuHanmu GuoWenqi ShanRong LiuZhiya GuTao WangPublished in: Oxidative medicine and cellular longevity (2022)
Traumatic brain injury (TBI) is a serious health issue with a high incidence, high morbidity, and high mortality that poses a large burden on society. Further understanding of the pathophysiology and cell death models induced by TBI may support targeted therapies for TBI patients. Ferroptosis, a model of programmed cell death first defined in 2012, is characterized by iron dyshomeostasis, lipid peroxidation, and glutathione (GSH) depletion. Ferroptosis is distinct from apoptosis, autophagy, pyroptosis, and necroptosis and has been shown to play a role in secondary brain injury and worsen long-term outcomes after TBI. This review systematically describes (1) the regulatory pathways of ferroptosis after TBI, (2) the neurobiological links between ferroptosis and other cell death models, and (3) potential therapies targeting ferroptosis for TBI patients.
Keyphrases
- cell death
- traumatic brain injury
- cell cycle arrest
- brain injury
- end stage renal disease
- severe traumatic brain injury
- healthcare
- chronic kidney disease
- newly diagnosed
- ejection fraction
- risk factors
- public health
- prognostic factors
- peritoneal dialysis
- mild traumatic brain injury
- type diabetes
- mental health
- signaling pathway
- risk assessment
- health information
- climate change
- cardiovascular events
- cerebral ischemia
- social media