Intracerebral hemorrhage is a life-threatening condition with a high fatality rate and severe sequelae. However, there is currently no treatment available for intracerebral hemorrhage, unlike for other stroke subtypes. Recent studies have indicated that mitochondrial dysfunction and mitophagy likely relate to the pathophysiology of intracerebral hemorrhage. Mitophagy, or selective autophagy of mitochondria, is an essential pathway to preserve mitochondrial homeostasis by clearing up damaged mitochondria. Mitophagy markedly contributes to the reduction of secondary brain injury caused by mitochondrial dysfunction after intracerebral hemorrhage. This review provides an overview of the mitochondrial dysfunction that occurs after intracerebral hemorrhage and the underlying mechanisms regarding how mitophagy regulates it, and discusses the new direction of therapeutic strategies targeting mitophagy for intracerebral hemorrhage, aiming to determine the close connection between mitophagy and intracerebral hemorrhage and identify new therapies to modulate mitophagy after intracerebral hemorrhage. In conclusion, although only a small number of drugs modulating mitophagy in intracerebral hemorrhage have been found thus far, most of which are in the preclinical stage and require further investigation, mitophagy is still a very valid and promising therapeutic target for intracerebral hemorrhage in the long run.
Keywords: intracerebral hemorrhage; mitochondrial dysfunction; mitophagy; neuroinflammation; neuroprotection; reactive oxygen species; secondary brain injury; therapeutic target.