title: Signaling Pathway in Early Brain Injury after Subarachnoid Hemorrhage: News Update.
abstract: The annual incidence of subarachnoid hemorrhage (SAH) caused by intracranial aneurysm rupture is approximately 10.5/10 million people in China, making SAH the third most frequently occurring hemorrhage of the intracranial type after cerebral embolism and hypertensive intracerebral hemorrhage. SAH caused by ruptured aneurysm leads to a mortality rate as high as 67 %, and, because of the sudden onset of this disease, approximately 12-15 % of patients die before they can receive effective treatment. Early brain injury (EBI) is the brain damage occurring within the first 72 h after SAH. Two-thirds of mortality caused by SAH occurs within 48 h, mainly as a result of EBI. With the development of molecular biology and medicine microscopy techniques, various signaling pathways involved in EBI after SAH have been revealed. Understanding these signaling pathways may help clinicians treat EBI after SAH and improve long-term prognosis of SAH patients. This chapter summarizes several important signaling pathways implicated in EBI caused by SAH.
authors.affiliation: Department of Neurosurgery, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, P. R. China.
authors.forename: Chengyuan
authors.initials: C
authors.lastname: Ji
authors.affiliation: Department of Neurosurgery, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, 215006, P. R. China. nju_neurosurgery@163.com.
authors.forename: Gang
authors.initials: G
authors.lastname: Chen
mesh_terms: D000818:Animals; D061745:Antioxidant Response Elements; D017209:Apoptosis / Q000502:physiology; D001343:Autophagy; D001812:Blood-Brain Barrier / Q000378:metabolism; D001921:Brain / Q000378:metabolism* / Q000503:physiopathology; D001929:Brain Edema / Q000378:metabolism* / Q000503:physiopathology; D002545:Brain Ischemia / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D007249:Inflammation; D000072019:Kelch-Like ECH-Associated Protein 1 / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D051267:NF-E2-Related Factor 2 / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D043684:Receptor, Adenosine A3 / Q000378:metabolism; D015398:Signal Transduction; D013345:Subarachnoid Hemorrhage / Q000378:metabolism* / Q000503:physiopathology; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism; D051193:Toll-Like Receptors / Q000378:metabolism
chemical_list: D000072019:Kelch-Like ECH-Associated Protein 1; D051267:NF-E2-Related Factor 2; D016328:NF-kappa B; D043684:Receptor, Adenosine A3; D051193:Toll-Like Receptors; D058570:TOR Serine-Threonine Kinases; D020928:Mitogen-Activated Protein Kinases
keywords: Autophagy; Early brain injury; Signaling pathway; Subarachnoid hemorrhage