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

Ehsan Dadgostar, Shiva Rahimi, Shahin Nikmanzar, Sina Nazemi, Mojtaba Naderi Taheri, Zahra Alibolandi, Michael Aschner, Hamed Mirzaei, Omid Reza Tamtaji

Research output: Contribution to journalReview articlepeer-review

10 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)860-871
Number of pages12
JournalNeurochemical Research
Issue number4
StatePublished - Apr 2022


  • Aquaporin 4
  • Edema
  • Molecular mechanisms
  • Targeted therapy
  • Traumatic brain injury

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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