ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2022
pH and proton-sensitive receptors in brain ischemia.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Potentiation of GPR68 alleviates post-ischemia BBB dysfunction and brain edema in mice.Experimental neurology · 2026Article
- Confined spaces in space: Cerebral implications of chronic elevations of inspired carbon dioxide and implications for long-duration space travel.Experimental physiology · 2026Review
- The Dual Roles of Microglia- and Astrocyte-Derived Exosomes in Cerebral Ischemia-Reperfusion Injury: from Intercellular Communication to Therapeutic Prospects.Molecular neurobiology · 2026Review
- Activation of the human β3 GABABiochemical pharmacology · 2026Article
- Proton-activated chloride channel 1 is essential for innate host defense against bacterial sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Structural Descriptors and Antioxidant Activity Markers of 4-[4-(2-Aminoethoxy)benzyl]aniline.Antioxidants (Basel, Switzerland) · 2026Article
- Article
- Properties of Acute Activation and Inhibition of the β3 Homomeric GABAACS chemical neuroscience · 2025Article
- Molecular mechanism of pH sensing and activation in GPR4 reveals proton-mediated GPCR signaling.Cell discovery · 2025Article
- A dangerous liaison: Spreading depolarization and tissue acidification in cerebral ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025Review
- Glu592 of the axon guidance receptor ROBO3 mediates a pH-dependent interaction with NELL2 ligand.FEBS letters · 2025Article
- Computation suggests that the cell adhesion sub-proteome is enriched for sites of pH-dependence and charge burial.PloS one · 2025Article
- Inhibition of acid-sensing receptor GPR4 attenuates neuronal ferroptosis via RhoA/YAP signaling in a rat model of subarachnoid hemorrhage.Free radical biology & medicine · 2024Article
- Time-Dependent Potentiation of the PERK Branch of UPR by GPR68 Offers Protection in Brain Ischemia.Stroke · 2024Article
- The plasma membrane inner leaflet PI(4,5)PNature communications · 2024Article
- Integrated Bulk and Single-Cell RNA-Sequencing Reveals the Effects of Circadian Rhythm Disruption on the Metabolic Reprogramming of CD4+ T Cells in Alzheimer's Disease.Molecular neurobiology · 2024Article
- Delayed Chronic Acidic Postconditioning Improves Poststroke Motor Functional Recovery and Brain Tissue Repair by Activating Proton-Sensing TDAG8.Translational stroke research · 2024Article
- Delivery-mediated exosomal therapeutics in ischemia-reperfusion injury: advances, mechanisms, and future directions.Nano convergence · 2024Review
- Bicarbonate signalling via G protein-coupled receptor regulates ischaemia-reperfusion injury.Nature communications · 2024Article
- High lactic acid levels in the brain contribute to the generation of focal slowing on the electroencephalogram.Frontiers in neurology · 2024Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Extracellular proton concentration is at 40 nM when pH is 7.4. In disease conditions such as brain ischemia, proton concentration can reach µM range. To respond to this increase in extracellular proton concentration, the mammalian brain expresses at least three classes of proton receptors. Acid-sensing ion channels (ASICs) are the main neuronal cationic proton receptor. The proton-activated chloride channel (PAC), which is also known as (aka) acid-sensitive outwardly rectifying anion channel (ASOR; TMEM206), mediates acid-induced chloride currents. Besides proton-activated channels, GPR4, GPR65 (aka TDAG8, T-cell death-associated gene 8), and GPR68 (aka OGR1, ovarian cancer G protein-coupled receptor 1) function as proton-sensitive G protein-coupled receptors (GPCRs). Though earlier studies on these GPCRs mainly focus on peripheral cells, we and others have recently provided evidence for their functional importance in brain injury. Specifically, GPR4 shows strong expression in brain endothelium, GPR65 is present in a fraction of microglia, while GPR68 exhibits predominant expression in brain neurons. Here, to get a better view of brain acid signaling and its contribution to ischemic injury, we will review the recent findings regarding the differential contribution of proton-sensitive GPCRs to cerebrovascular function, neuroinflammation, and neuronal injury following acidosis and brain ischemia.
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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.