Mitophagy and Traumatic Brain Injury: Regulatory Mechanisms and Therapeutic Potentials.
Yi LuanLulu JiangYing LuanYi XieYang YangKai-Di RenPublished in: Oxidative medicine and cellular longevity (2023)
Traumatic brain injury (TBI), a kind of external trauma-induced brain function alteration, has posed a financial burden on the public health system. TBI pathogenesis involves a complicated set of events, including primary and secondary injuries that can cause mitochondrial damage. Mitophagy, a process in which defective mitochondria are specifically degraded, segregates and degrades defective mitochondria allowing a healthier mitochondrial network. Mitophagy ensures that mitochondria remain healthy during TBI, determining whether neurons live or die. Mitophagy acts as a critical regulator in maintaining neuronal survival and healthy. This review will discuss the TBI pathophysiology and the consequences of the damage it causes to mitochondria. This review article will explore the mitophagy process, its key factors, and pathways and reveal the role of mitophagy in TBI. Mitophagy will be further recognized as a therapeutic approach in TBI. This review will offer new insights into mitophagy's role in TBI progression.
Keyphrases
- traumatic brain injury
- nlrp inflammasome
- severe traumatic brain injury
- oxidative stress
- cell death
- mild traumatic brain injury
- reactive oxygen species
- endoplasmic reticulum
- healthcare
- mental health
- multiple sclerosis
- emergency department
- gene expression
- spinal cord injury
- endothelial cells
- white matter
- dna methylation
- high glucose
- young adults
- drug induced