title: The Role of Autophagy in Subarachnoid Hemorrhage: An Update.
abstract: 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 SAH.
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
authors.forename: Yuanjian
authors.initials: Y
authors.lastname: Fang
authors.affiliation: Department of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
authors.forename: Sheng
authors.initials: S
authors.lastname: Chen
authors.affiliation: Department of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, United States.|Department of Preventive Medicine, Loma Linda University Medical Center, Loma Linda, CA, United States.
authors.forename: Cesar
authors.initials: C
authors.lastname: Reis
authors.affiliation: Department of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.|Brain Research Institute, Zhejiang University, Hangzhou, Zhejiang, China.|Collaborative Innovation Center for Brain Science, Zhejiang University, Hangzhou, Zhejiang, China.
authors.forename: Jianmin
authors.initials: J
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001343:Autophagy; D006801:Humans; D013345:Subarachnoid Hemorrhage / Q000503:physiopathology*
keywords: Autophagy; early brain injury; pathogenesis; subarachnoid hemorrhage; subcellular organelles; treatment.