Acute central nervous system injuries, including ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, traumatic brain injury, and spinal cord injury, are a major global health challenge. Identifying optimal therapies and improving the long-term neurological functions of patients with acute central nervous system injuries are urgent priorities. Mitochondria are susceptible to damage after acute central nervous system injury, and this leads to the release of toxic levels of reactive oxygen species, which induce cell death. Mitophagy, a selective form of autophagy, is crucial in eliminating redundant or damaged mitochondria during these events. Recent evidence has highlighted the significant role of mitophagy in acute central nervous system injuries. In this review, we provide a comprehensive overview of the process, classification, and related mechanisms of mitophagy. We also highlight the recent developments in research into the role of mitophagy in various acute central nervous system injuries and drug therapies that regulate mitophagy. In the final section of this review, we emphasize the potential for treating these disorders by focusing on mitophagy and suggest future research paths in this area.
Keyphrases
- cell death
- liver failure
- cerebrospinal fluid
- subarachnoid hemorrhage
- nlrp inflammasome
- respiratory failure
- reactive oxygen species
- drug induced
- traumatic brain injury
- spinal cord injury
- brain injury
- aortic dissection
- global health
- oxidative stress
- public health
- transcription factor
- emergency department
- machine learning
- signaling pathway
- intensive care unit
- spinal cord
- extracorporeal membrane oxygenation