The role of autophagy and apoptosis in early brain injury after subarachnoid hemorrhage: an updated review.

Subarachnoid hemorrhage (SAH) is a worldwide devastating type of stroke with high mortality and morbidity. Accumulating evidence show early brain injury (EBI) as the leading cause of mortality after SAH. The pathological processes involved in EBI include decreased cerebral blood flow, increased intracranial pressure, vasospasm, and disruption of the blood-brain barrier. In addition, neuroinflammation, oxidative stress, apoptosis, and autophagy have also been proposed to contribute to EBI. Among the various processes involved in EBI, neuronal apoptosis has been proven to be a key factor contributing to the poor prognosis of SAH patients. Meanwhile, as another important catabolic process maintaining the cellular and tissue homeostasis, autophagy has been shown to be neuroprotective after SAH. Studies have shown that enhancing autophagy reduced apoptosis, whereas inhibiting autophagy aggravate neuronal apoptosis after SAH. The physiological substrates and mechanisms of neuronal autophagy and apoptosis by which defects in neuronal function are largely unknown. In this review, we summarize and discuss the role of autophagy and apoptosis after SAH and contribute to further study for investigation of the means to control the balance between them.