|
|||||
|
|
Aquaporin 4 in Traumatic Brain Injury: From Molecular Pathways to Therapeutic Target |
|
| Authors: | Dadgostar Ehsan Rahimi Shiva Nikmanzar Shahin Nazemi Sina Naderi Taheri Mojtaba Alibolandi Zahra Aschner Michael Mirzaei Hamed Tamtaji Omid Reza |
| Institution: | 1.Behavioral Sciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran ;2.Student Research Committee, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran ;3.School of Medicine, Fasa University of Medical Sciences, Fasa, Iran ;4.Department of Neurosurgery, Iran University of Medical Sciences, Tehran, Iran ;5.Tracheal Disease Research Center (TDRC), National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran ;6.Students’ Scientific Research Center (SSRC), Tehran University of Medical Sciences, Tehran, Iran ;7.Anatomical Science Research Center, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, Iran ;8.Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY, 10461, USA ;9.Research Center for Biochemistry and Nutrition in Metabolic Diseases, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, Iran ; |
| 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. |
| Keywords: | |
| 本文献已被 SpringerLink 等数据库收录！ | |