title: Progress in AQP Research and New Developments in Therapeutic Approaches to Ischemic and Hemorrhagic Stroke.
abstract: Cerebral edema often manifests after the development of cerebrovascular disease, particularly in the case of stroke, both ischemic and hemorrhagic. Without clinical intervention, the influx of water into brain tissues leads to increased intracranial pressure, cerebral herniation, and ultimately death. Strategies to manage the development of edema constitute a major unmet therapeutic need. However, despite its major clinical significance, the mechanisms underlying cerebral water transport and edema formation remain elusive. Aquaporins (AQPs) are a class of water channel proteins which have been implicated in the regulation of water homeostasis and cerebral edema formation, and thus represent a promising target for alleviating stroke-induced cerebral edema. This review examines the significance of relevant AQPs in stroke injury and subsequently explores neuroprotective strategies aimed at modulating AQP expression, with a particular focus on AQP4, the most abundant AQP in the central nervous system.
authors.affiliation: Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI 48201, USA. lprevich@med.wayne.edu.
authors.forename: Lauren E
authors.initials: LE
authors.lastname: Previch
authors.affiliation: Department of Neurology, Beijing Luhe Hospital, Capital Medical University, Beijing 101199, China. hotmoonml@hotmail.com.
authors.forename: Linlin
authors.initials: L
authors.lastname: Ma
authors.affiliation: Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI 48201, USA. jowright@med.wayne.edu.
authors.forename: Joshua C
authors.initials: JC
authors.lastname: Wright
authors.affiliation: Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI 48201, USA. sunpreet.singh94@gmail.com.
authors.forename: Sunpreet
authors.initials: S
authors.lastname: Singh
authors.affiliation: Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI 48201, USA. xgeng@ccmu.edu.cn.|Department of Neurology, Beijing Luhe Hospital, Capital Medical University, Beijing 101199, China. xgeng@ccmu.edu.cn.|China-America Institute of Neuroscience, Beijing Luhe Hospital, Capital Medical University, Beijing 101199, China. xgeng@ccmu.edu.cn.
authors.forename: Xiaokun
authors.initials: X
authors.lastname: Geng
authors.affiliation: Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI 48201, USA. yding@med.wayne.edu.|China-America Institute of Neuroscience, Beijing Luhe Hospital, Capital Medical University, Beijing 101199, China. yding@med.wayne.edu.
authors.forename: Yuchuan
authors.initials: Y
authors.lastname: Ding
mesh_terms: D020346:Aquaporins / Q000378:metabolism*; D002545:Brain Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D002543:Cerebral Hemorrhage / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D020521:Stroke / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology
chemical_list: D020346:Aquaporins
keywords: aquaporin; cytotoxic edema; hemorrhagic stroke; ischemic stroke; vasogenic edema