ArticleCNS neuroscience & therapeutics2012
AQP4 knockout aggravates ischemia/reperfusion injury in mice.
Article in CNS neuroscience & therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 60 citations in OpenAlex.
- Aquaporin-4 in Stroke and Brain Edema-Friend or Foe?International journal of molecular sciences · 2025Review
- Hybrid Electro-optical Stimulation Improves Ischemic Brain Damage by Augmenting the Glymphatic System.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A novel annexin dimer targets microglial phagocytosis of astrocytes to protect the brain-blood barrier after cerebral ischemia.Acta pharmacologica Sinica · 2025Article
- Astrocyte Dysfunction Reflected in Ischemia-Induced Astrocyte-Derived Extracellular Vesicles: A Pilot Study on Acute Ischemic Stroke Patients.International journal of molecular sciences · 2024Article
- Astrocytes in functional recovery following central nervous system injuries.The Journal of physiology · 2024Review
- Role of the glymphatic system and perivascular spaces as a potential biomarker for post-stroke epilepsy.Epilepsia open · 2024Review
- Stroke and Neurogenesis: Bridging Clinical Observations to New Mechanistic Insights from Animal Models.Translational stroke research · 2024Review
- Aquaporin-4 and Parkinson's Disease.International journal of molecular sciences · 2024Review
- Exploring Astrocyte-Mediated Mechanisms in Sleep Disorders and Comorbidity.Biomedicines · 2023Review
- Molecular mechanism of cerebral edema improvement via IL-1RA released from the stroke-unaffected hindlimb by treadmill exercise after cerebral infarction in rats.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- The lymphatic drainage systems in the brain: a novel target for ischemic stroke?Neural regeneration research · 2023Review
- Astrocytes in stroke-induced neurodegeneration: a timeline.Frontiers in molecular medicine · 2023Review
- Stroke-induced damage on the blood-brain barrier.Frontiers in neurology · 2023Review
- Role of astrocytes in sleep deprivation: accomplices, resisters, or bystanders?Frontiers in cellular neuroscience · 2023Review
- Elevated Intracranial Pressure in Cryptococcal Meningoencephalitis: Examining Old, New, and Promising Drug Therapies.Pathogens (Basel, Switzerland) · 2022Review
- The mechanisms underlying the actions of Xuefu Zhuyu decoction pretreatment against neurological deficits after ischemic stroke in mice: The mediation of glymphatic function by aquaporin-4 and its anchoring proteins.Frontiers in pharmacology · 2022Article
- The role of circadian clock in astrocytes: From cellular functions to ischemic stroke therapeutic targets.Frontiers in neuroscience · 2022Review
- The absence of AQP4/TRPV4 complex substantially reduces acute cytotoxic edema following ischemic injury.Frontiers in cellular neuroscience · 2022Article
- Aquaporin 4 inhibition alleviates myocardial ischemia-reperfusion injury by restraining cardiomyocyte pyroptosis.Bioengineered · 2021Article
- Aquaporin 4 and brain-related disorders: Insights into its apoptosis roles.EXCLI journal · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeThe glial water channel aquaporin-4 (AQP4) has been shown to be involved in a wide range of brain disorders. Although its important role in stroke has already been documented, the underlying mechanism was not clarified yet. Therefore, this study was designed to investigate the impacts of AQP4 deletion in ischemia/reperfusion (I/R). METHODS AND
resultsHerein we found a higher mortality and more severe neurological deficits in AQP4 knockout (AQP4(-/-)) mice after transient middle cerebral artery occlusion while no difference was observed in water content variation during I/R between two genotypes except a higher basal water content developed in AQP4(-/-) mouse brain, implying the same increment of water content over a higher basal level may provoke an even more elevated intracranial pressure, which might be an important cause of increased mortality in AQP4(-/-) mice. Moreover, AQP4 knockout aggravated I/R injury with enlarged infarct size and a more serious loss of CA1 neurons accompanied by a striking hypertrophy of astrocytes, suggesting an involvement of AQP4 in astrocytic dysfunction.
conclusionsOur findings provide direct evidence that AQP4 plays a crucial role in the pathogenesis of I/R injury, which may confer a new option for stroke treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.