ArticleJournal of neuroinflammation2017
The potassium channel KCa3.1 constitutes a pharmacological target for astrogliosis associated with ischemia stroke.
Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- PHPT1 acts as an inhibitor in high-altitude pulmonary hypertension via negative TRPV5 signaling regulation.Journal of translational medicine · 2025Article
- Article
- Neonatal Chlamydia muridarum respiratory infection causes neuroinflammation within the brainstem during the early postnatal period.Journal of neuroinflammation · 2024Article
- Ion Channels and Ionotropic Receptors in Astrocytes: Physiological Functions and Alterations in Alzheimer's Disease and Glioblastoma.Life (Basel, Switzerland) · 2023Review
- Astrocytic TRPV4 Channels and Their Role in Brain Ischemia.International journal of molecular sciences · 2023Review
- Ion Channel Dysfunction in Astrocytes in Neurodegenerative Diseases.Frontiers in physiology · 2022Review
- The potassium channel KCa3.1 represents a valid pharmacological target for microgliosis-induced neuronal impairment in a mouse model of Parkinson's disease.Journal of neuroinflammation · 2019Article
- Megalencephalic Leukoencephalopathy with Subcortical Cysts Protein-1 (MLC1) Counteracts Astrocyte Activation in Response to Inflammatory Signals.Molecular neurobiology · 2019Article
- Augmented astrocyte microdomain CaGlia · 2019Article
- Neurovascular unit transport responses to ischemia and common coexisting conditions: smoking and diabetes.American journal of physiology. Cell physiology · 2019Review
- CaJournal of neuroinflammation · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundReactive astrogliosis is one of the significantly pathological features in ischemic stroke accompanied with changes in gene expression, morphology, and proliferation. KCa3.1 was involved in TGF-β-induced astrogliosis in vitro and also contributed to astrogliosis-mediated neuroinflammation in neurodegeneration disease.
methodsWild type mice and KCa3.1
resultsImmunohistochemistry on pMCAO mice infarcts showed strong upregulation of KCa3.1 immunoreactivity in reactive astrogliosis. KCa3.1
conclusionsOur data suggested that KCa3.1 inhibition might represent a promising therapeutic strategy for ischemia stroke.
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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.