ReviewFrontiers in cellular neuroscience2018
It's All about Timing: The Involvement of Kir4.1 Channel Regulation in Acute Ischemic Stroke Pathology.
Review in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Selective Deletion of NBCe1 in Reactive Astrocytes Attenuates Ischemic Stroke Brain Damage.Glia · 2025Article
- Channels and Transporters in Ischemic Brain Edema.Journal of inflammation research · 2025Review
- Article
- Yigan Mingmu Decoction inhibits diabetic macular edema through regulating Kir4.1/AQP4 axis: a study based on network pharmacology.American journal of translational research · 2023Article
- VU6036720: The First Potent and Selective In Vitro Inhibitor of Heteromeric Kir4.1/5.1 Inward Rectifier Potassium Channels.Molecular pharmacology · 2022Article
- New Candidates for Biomarkers and Drug Targets of Ischemic Stroke-A First Dynamic LC-MS Human Serum Proteomic Study.Journal of clinical medicine · 2022Article
- A Bibliometric Analysis for Global Trends and Full View of the Autophagy in Ischemic Stroke from 2006 to 2022.BioMed research international · 2022Article
- Astrocytes profiling in acute hepatic encephalopathy: Possible enrolling of glial fibrillary acidic protein, tumor necrosis factor-alpha, inwardly rectifying potassium channel (Kir 4.1) and aquaporin-4 in rat cerebral cortex.Frontiers in cellular neuroscience · 2022Article
- Article
- Kir4.1 may represent a novel therapeutic target for diabetic retinopathy (Review).Experimental and therapeutic medicine · 2021Review
- Dysregulation of Astrocyte Ion Homeostasis and Its Relevance for Stroke-Induced Brain Damage.International journal of molecular sciences · 2021Review
- Nutritional ketosis as an intervention to relieve astrogliosis: Possible therapeutic applications in the treatment of neurodegenerative and neuroprogressive disorders.European psychiatry : the journal of the Association of European Psychiatrists · 2020Review
- Effect of Ibuprofen on Autophagy of Astrocytes During Pentylenetetrazol-Induced Epilepsy and its Significance: An Experimental Study.Neurochemical research · 2019Article
- MK-801 attenuates lesion expansion following acute brain injury in rats: a meta-analysis.Neural regeneration research · 2019Article
- Age-dependent alterations of Kir4.1 expression in neural crest-derived cells of the mouse and human cochlea.Neurobiology of aging · 2019Article
- Bursting at the Seams: Molecular Mechanisms Mediating Astrocyte Swelling.International journal of molecular sciences · 2019Review
- Involvement of extrasynaptic glutamate in physiological and pathophysiological changes of neuronal excitability.Cellular and molecular life sciences : CMLS · 2018Review
- A Purinergic P2 Receptor Family-Mediated Increase in Thrombospondin-1 Bolsters Synaptic Density and Epileptic Seizure Activity in the Amygdala-Kindling Rat Model.Frontiers in cellular neuroscience · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An acute ischemic stroke is characterized by the presence of a blood clot that limits blood flow to the brain resulting in subsequent neuronal loss. Acute stroke threatens neuronal survival, which relies heavily upon proper function of astrocytes. Neurons are more susceptible to cell death when an astrocyte is unable to carry out its normal functions in supporting the neuron in the area affected by the stroke (Rossi et al., 2007; Takano et al., 2009). For example, under normal conditions, astrocytes initially swell in response to changes in extracellular osmotic pressure and then reduce their regulatory volume in response to volume-activated potassium (K
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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.