Mitochondria as a therapeutic target for ischemic stroke

Stroke is the leading cause of death and physical disability worldwide. Mitochondrial dysfunction has been considered as one of the hallmarks of ischemic stroke and contributes to the pathology of ischemia and re-perfusion. Mitochondria is essential in promoting neural survival and neurological improvement following ischemic stroke. Therefore, mitochondria represent an important drug target for stroke treatment. This review discusses the mitochondrial molecular mechanisms underlying cerebral ischemia and involved in reactive oxygen species generation, mitochondrial electron transport dysfunction, mitochondria-mediated regulation of inflammasome activation, mitochondrial dynamics and biogenesis, and apoptotic cell death. We highlight the potential of mitochondrial transfer by stem cells as a therapeutic target for stroke treatment and provide valuable insights for clinical strategies. A better understanding of the roles of mitochondria in ischemia-induced cell death and protection may provide a rationale design of novel therapeutic interventions in the ischemic stroke.