ReviewActa pharmacologica Sinica2013
Chloride channels in stroke.
Review in Acta pharmacologica Sinica, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- A novel nomogram to predict mortality in patients with stroke: a survival analysis based on the MIMIC-III clinical database.BMC medical informatics and decision making · 2022Trial
- Loss of Vascular TMEM16A Impairs Cerebral Autoregulation and Exacerbates Ischemia-reperfusion Injury.Translational stroke research · 2026Article
- Article
- Commentary for the article: MicroRNA-1246 regulates proliferation, invasion and differentiation in human vascular smooth muscle cell by targeting cystic fibrosis transmembrane conductance regulator (CFTR).Pflugers Archiv : European journal of physiology · 2021Article
- Drug development in targeting ion channels for brain edema.Acta pharmacologica Sinica · 2020Article
- CFTR prevents neuronal apoptosis following cerebral ischemia reperfusion via regulating mitochondrial oxidative stress.Journal of molecular medicine (Berlin, Germany) · 2018Article
- Fluid shear stress enhances the cell volume decrease of osteoblast cells by increasing the expression of the ClC-3 chloride channel.Biomedical reports · 2016Article
- High fructose causes cardiac hypertrophy via mitochondrial signaling pathway.American journal of translational research · 2016Article
- Identification and characterization of a novel promoter for the human ANO1 gene regulated by the transcription factor signal transducer and activator of transcription 6 (STAT6).FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Common mechanisms of Alzheimer's disease and ischemic stroke: the role of protein kinase C in the progression of age-related neurodegeneration.Journal of Alzheimer's disease : JAD · 2015Review
- Controversies and evolving new mechanisms in subarachnoid hemorrhage.Progress in neurobiology · 2014Article
- ClC-3 chloride channel in hippocampal neuronal apoptosis.Neural regeneration research · 2013Article
- Sphingosine and FTY720 modulate pacemaking activity in interstitial cells of Cajal from mouse small intestine.Molecules and cells · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Vascular remodeling of cerebral arterioles, including proliferation, migration, and apoptosis of vascular smooth muscle cells (VSMCs), is the major cause of changes in the cross-sectional area and diameter of the arteries and sudden interruption of blood flow or hemorrhage in the brain, ie, stroke. Accumulating evidence strongly supports an important role for chloride (Cl(-)) channels in vascular remodeling and stroke. At least three Cl(-) channel genes are expressed in VSMCs: 1) the TMEM16A (or Ano1), which may encode the calcium-activated Cl(-) channels (CACCs); 2) the CLC-3 Cl(-) channel and Cl(-)/H(+) antiporter, which is closely related to the volume-regulated Cl(-) channels (VRCCs); and 3) the cystic fibrosis transmembrane conductance regulator (CFTR), which encodes the PKA- and PKC-activated Cl(-) channels. Activation of the CACCs by agonist-induced increase in intracellular Ca(2+) causes membrane depolarization, vasoconstriction, and inhibition of VSMC proliferation. Activation of VRCCs by cell volume increase or membrane stretch promotes the production of reactive oxygen species, induces proliferation and inhibits apoptosis of VSMCs. Activation of CFTR inhibits oxidative stress and may prevent the development of hypertension. In addition, Cl(-) current mediated by gamma-aminobutyric acid (GABA) receptor has also been implicated a role in ischemic neuron death. This review focuses on the functional roles of Cl(-) channels in the development of stroke and provides a perspective on the future directions for research and the potential to develop Cl(-) channels as new targets for the prevention and treatment of stroke.
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Identifiers
What OpenQuestion holds
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.