Background: Autophagy is an extensive self-degradation process for the disposition of
cytosolic aggregated or misfolded proteins and defective organelles which executes the functions
of pro-survival and pro-death to maintain cellular homeostasis. The pathway plays essential roles
in several neurological disorders. Subarachnoid Hemorrhage (SAH) is a devastating subtype of
hemorrhagic stroke with high risk of neurological deficit and high mortality. Early brain injury
(EBI) plays a role in the poor clinical course and outcome after SAH. Recent studies have paid
attention on the role of the autophagy pathway in the development of EBI after SAH. We aim to
update the multifaceted roles of autophagy pathway in the pathogenesis of SAH, especially in the
phase of EBI.
Methods: We reviewed early researches related to autophagy and SAH. The following three
aspects of contents will be mainly discussed: the process of the autophagy pathway, the role of the
autophagy in SAH and the interaction between organelle dysfunction and autophagy pathway after
Results: Accumulating evidence shows an increased autophagy reaction in response to early stages
of SAH. However, others suggest inadequate or excessive autophagy activation can result in cell
injury and death. In addition to autophagy, apoptosis and necrosis can occur in neurons simultaneously
after SAH, leading to mixed features of cell death morphologies. And it is also known that
there is extensive crosstalk between autophagy and apoptosis pathway. Subcellular organelles of
neural cells generally participate in the formation and functional parts of autophagy process.
Conclusion: Autophagy plays an important role in the SAH-induced brain injury. A better
understanding of the interrelationship among autophagy, apoptosis, and necrosis might provide us
better therapeutic targets for the treatment of SAH.