Aquaporin 4 in Traumatic Brain Injury: From Molecular Pathways to Therapeutic Target Publisher Pubmed



Dadgostar E^{1, 2} ; Rahimi S³ ; Nikmanzar S⁴ ; Nazemi S⁵ ; Naderi Taheri M⁶ ; Alibolandi Z⁷ ; Aschner M⁸ ; Mirzaei H⁹ ; Tamtaji OR⁶ Show Affiliations
Source: Neurochemical Research Published:2022

Abstract

Traumatic brain injury (TBI) is known as an acute degenerative pathology of the central nervous system, and has been shown to increase brain aquaporin 4 (AQP4) expression. Various molecular mechanisms affect AQP4 expression, including neuronal high mobility group box 1, forkhead box O3a, vascular endothelial growth factor, hypoxia-inducible factor-1 α (HIF-1 α) sirtuin 2, NF-κB, Malat1, nerve growth factor and Angiotensin II receptor type 1. In addition, inhibition of AQP4 with FK-506, MK-801 (indirectly by targeting N-methyl-d-aspartate receptor), inactivation of adenosine A2A receptor, levetiracetam, adjudin, progesterone, estrogen, V1aR inhibitor, hypertonic saline, erythropoietin, poloxamer 188, brilliant blue G, HIF-1alpha inhibitor, normobaric oxygen therapy, astaxanthin, epigallocatechin-3-gallate, sesamin, thaliporphine, magnesium, prebiotic fiber, resveratrol and omega-3, as well as AQP4 gene silencing lead to reduced edema upon TBI. This review summarizes current knowledge and evidence on the relationship between AQP4 and TBI, and the potential mechanisms involved. © 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.