• T Peeyush Kumar, Devin W McBride, Pramod K Dash, Kanako Matsumura, Alba Rubi, and Spiros L Blackburn.
• The Vivian L. Smith Department of Neurosurgery, University of Texas Health Science Center, 6431 Fannin St., Houston, TX, 77030, USA. Peeyush.K.Thankamanipandit@uth.tmc.edu.
• Mol. Neurobiol. 2019 Mar 1; 56 (3): 1992-2006.

AbstractIn the brain, vascular endothelial cells conserve blood viscosity, control blood flow, and form the interface between central nervous system and circulating blood. Clinical outcome after aneurysmal subarachnoid hemorrhage is linked to early brain injury, cerebral vasospasm, and other causes of delayed cerebral ischemia. The cerebral vasculature remains a unique target for therapies since it becomes rapidly disrupted after subarachnoid hemorrhage, and damage to the blood vessels continues into the delayed injury phase. The current failure of therapies to improve clinical outcome warrants a re-evaluation of current therapeutic approaches. The mechanisms of endothelial cell injury and blood-brain barrier breakdown are critical to the pathway of cerebral injury, and an improved understanding of these mechanisms may lead to novel therapeutic targets. This review provides an update on the current understanding of endothelial cell injury following aneurysmal subarachnoid hemorrhage, including blood-brain barrier dysfunction.

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