ArticlePloS one2012
Deletion of TRAAK potassium channel affects brain metabolism and protects against ischemia.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
21 citing papers in PubMed.
- K2P channels as emerging therapeutic targets for pain: insights from functional studies and transcriptomic analyses.Frontiers in pharmacology · 2026Review
- Unraveling the Molecular Reason of Opposing Effects of α-Mangostin and Norfluoxetine on TREK-2 at the Same Binding Site.ChemMedChem · 2024Article
- Research progress of two-pore potassium channel in myocardial ischemia-reperfusion injury.Frontiers in physiology · 2024Review
- Modulation of Mechanosensitive Potassium Channels by a Membrane-targeted Nongenetic Photoswitch.The journal of physical chemistry. B · 2023Article
- The Two-Pore Domain Potassium Channel TREK-1 Promotes Blood-Brain Barrier Breakdown and Exacerbates Neuronal Death After Focal Cerebral Ischemia in Mice.Molecular neurobiology · 2022Article
- Two-Pore-Domain Potassium (KCells · 2021Review
- Structural Insights into the Mechanisms and Pharmacology of KJournal of molecular biology · 2021Review
- The Polysite Pharmacology of TREK KAdvances in experimental medicine and biology · 2021Article
- Polynuclear Ruthenium Amines Inhibit KCell chemical biology · 2020Article
- Tandem pore TWIK-related potassium channels and neuroprotection.Neural regeneration research · 2019Review
- Neurovascular unit transport responses to ischemia and common coexisting conditions: smoking and diabetes.American journal of physiology. Cell physiology · 2019Review
- Protein and Chemical Determinants of BL-1249 Action and Selectivity for KACS chemical neuroscience · 2018Article
- TREK‑TRAAK two‑pore domain potassium channels protect human retinal pigment epithelium cells from oxidative stress.International journal of molecular medicine · 2018Article
- Mutations in KCNK4 that Affect Gating Cause a Recognizable Neurodevelopmental Syndrome.American journal of human genetics · 2018Article
- Creatine, Glutamine plus Glutamate, and Macromolecules Are Decreased in the Central White Matter of Premature Neonates around Term.PloS one · 2016Article
- Molecular mechanisms of temperature adaptation.The Journal of physiology · 2015Review
- The family of K2P channels: salient structural and functional properties.The Journal of physiology · 2015Review
- The CNS under pathophysiologic attack--examining the role of K₂p channels.Pflugers Archiv : European journal of physiology · 2015Review
- Augmentation of M-type (KCNQ) potassium channels as a novel strategy to reduce stroke-induced brain injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Temperature sensitivity of two-pore (K2P) potassium channels.Current topics in membranes · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral stroke is a worldwide leading cause of disability. The two-pore domain K⁺ channels identified as background channels are involved in many functions in brain under physiological and pathological conditions. We addressed the hypothesis that TRAAK, a mechano-gated and lipid-sensitive two-pore domain K⁺ channel, is involved in the pathophysiology of brain ischemia. We studied the effects of TRAAK deletion on brain morphology and metabolism under physiological conditions, and during temporary focal cerebral ischemia in Traak⁻/⁻ mice using a combination of in vivo magnetic resonance imaging (MRI) techniques and multinuclear magnetic resonance spectroscopy (MRS) methods. We provide the first in vivo evidence establishing a link between TRAAK and neurometabolism. Under physiological conditions, Traak⁻/⁻ mice showed a particular metabolic phenotype characterized by higher levels of taurine and myo-inositol than Traak⁺/⁺ mice. Upon ischemia, Traak⁻/⁻ mice had a smaller infarcted volume, with lower contribution of cellular edema than Traak⁺/⁺ mice. Moreover, brain microcirculation was less damaged, and brain metabolism and pH were preserved. Our results show that expression of TRAAK strongly influences tissue levels of organic osmolytes. Traak⁻/⁻ mice resilience to cellular edema under ischemia appears related to their physiologically high levels of myo-inositol and of taurine, an aminoacid involved in the modulation of mitochondrial activity and cell death. The beneficial effects of TRAAK deletion designate this channel as a promising pharmacological target for the treatment against stroke.
Indexed as
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.