TY - CHAP
T1 - Neurovascular events after subarachnoid hemorrhage
T2 - Focusing on subcellular organelles
AU - Chen, Sheng
AU - Wu, Haijian
AU - Tang, Jiping
AU - Zhang, Jianmin
AU - Zhang, John H.
N1 - Part of the Acta Neurochirurgica Supplement book series (NEUROCHIRURGICA, volume 120) Subarachnoid hemorrhage (SAH) is a devastating condition with high morbidity and mortality rates due to the lack of effective therapy. Early brain injury (EBI) and cerebral vasospasm (CVS) are the two most important pathophysiological mechanisms for brain injury and poor outcomes for patients with SAH.
PY - 2014/1/1
Y1 - 2014/1/1
N2 - Subarachnoid hemorrhage (SAH) is a devastating condition with high morbidity and mortality rates due to the lack of effective therapy. Early brain injury (EBI) and cerebral vasospasm (CVS) are the two most important pathophysiological mechanisms for brain injury and poor outcomes for patients with SAH. CVS has traditionally been considered the sole cause of delayed ischemic neurological defi cits after SAH. However, the failure of antivasospastic therapy in patients with SAH supported changing the research target from CVS to other mechanisms. Currently, more attention has been focused on global brain injury within 3 days after ictus, designated as EBI. The dysfunction of subcellular organelles, such as endoplasmic reticulum stress, mitochondrial failure, and autophagy–lysosomal system activation, has developed during EBI and delayed brain injury after SAH. To our knowledge, there is a lack of review articles addressing the direction of organelle dysfunction after SAH. In this review, we discuss the roles of organelle dysfunction in the pathogenesis of SAH and present the opportunity to develop novel therapeutic strategies of SAH via modulating the functions of organelles.
AB - Subarachnoid hemorrhage (SAH) is a devastating condition with high morbidity and mortality rates due to the lack of effective therapy. Early brain injury (EBI) and cerebral vasospasm (CVS) are the two most important pathophysiological mechanisms for brain injury and poor outcomes for patients with SAH. CVS has traditionally been considered the sole cause of delayed ischemic neurological defi cits after SAH. However, the failure of antivasospastic therapy in patients with SAH supported changing the research target from CVS to other mechanisms. Currently, more attention has been focused on global brain injury within 3 days after ictus, designated as EBI. The dysfunction of subcellular organelles, such as endoplasmic reticulum stress, mitochondrial failure, and autophagy–lysosomal system activation, has developed during EBI and delayed brain injury after SAH. To our knowledge, there is a lack of review articles addressing the direction of organelle dysfunction after SAH. In this review, we discuss the roles of organelle dysfunction in the pathogenesis of SAH and present the opportunity to develop novel therapeutic strategies of SAH via modulating the functions of organelles.
KW - Cerebral vasospasm
KW - Early brain injury
KW - Organelles
KW - Subarachnoid Hemorrhage
KW - Therapy
KW - Subarachnoid Hemorrhage/complications
KW - Organelles/pathology
KW - Signal Transduction
KW - Humans
KW - Brain Injuries/etiology
KW - Vasospasm, Intracranial/etiology
UR - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4373344/
UR - https://link.springer.com/content/pdf/10.1007%2F978-3-319-04981-6_7.pdf
UR - https://www.mendeley.com/catalogue/eb5948c2-330e-3cbe-b0a1-d2d9e658909b/
U2 - 10.1007/978-3-319-04981-6_7
DO - 10.1007/978-3-319-04981-6_7
M3 - Chapter
C2 - 25366597
VL - 120
T3 - Acta Neurochirurgica, Supplementum
SP - 39
EP - 46
BT - Neurovascular Events After Subarachnoid Hemorrhage
ER -