| Literature DB >> 30791865 |
Muyassar Mamtilahun1, Guanghui Tang2, Zhijun Zhang1, Yongting Wang1, Yaohui Tang1, Guo-Yuan Yang1,3.
Abstract
Brain edema primarily occurs as a consequence of various cerebral injuries including ischemic stroke. Excessive accumulation of brain water content causes a gradual expansion of brain parenchyma, decreased blood flow and increased intracranial pressure and, ultimately, cerebral herniation and death. Current clinical treatment for ischemic edema is very limited, therefore, it is urgent to develop novel treatment strategies. Mounting evidence has demonstrated that AQP4, a water channel protein, is closely correlated with brain edema and could be an optimal therapeutic target for the reduction of ischemic brain edema. AQP4 is prevalently distributed in the central nervous system, and mainly regulates water flux in brain cells under normal and pathological conditions. This review focuses on the underlying mechanisms of AQP4 related to its dual role in edema formation and elimination. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Entities:
Keywords: Aquaporin-4; brain edema; central nervous system; stroke; therapeutic target; water channel.
Year: 2019 PMID: 30791865 DOI: 10.2174/1389450120666190214115309
Source DB: PubMed Journal: Curr Drug Targets ISSN: 1389-4501 Impact factor: 3.465