ReviewThe Journal of physiology2015
Pannexin channels and ischaemia.
Review in The Journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 52 citations in OpenAlex.
- Dual Regulatory Roles of Pannexin 1 in the Pathogenesis and Recovery of Sepsis-Induced Acute Lung Injury.Infection and drug resistance · 2025Review
- Pannexin1 Channel-Mediated Inflammation in Acute Ischemic Stroke.Aging and disease · 2024Review
- Proteomic association with age-dependent sex differences in Wisconsin Card Sorting Test performance in healthy Thai subjects.Scientific reports · 2023Article
- Intra-carotid body inter-cellular communication.Journal of the Royal Society of New Zealand · 2023Review
- Pannexin 1 activity in astroglia sets hippocampal neuronal network patterns.PLoS biology · 2022Article
- Connexins and Pannexins: Important Players in Neurodevelopment, Neurological Diseases, and Potential Therapeutics.Biomedicines · 2022Review
- Signaling pathways involved in ischemic stroke: molecular mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2022Review
- The Critical Role of Spreading Depolarizations in Early Brain Injury: Consensus and Contention.Neurocritical care · 2022Review
- Article
- Myeloid Pannexin-1 mediates acute leukocyte infiltration and leads to worse outcomes after brain trauma.Journal of neuroinflammation · 2020Article
- Sarcoma Family Kinase-Dependent Pannexin-1 Activation after Cortical Spreading Depression is Mediated by NR2A-Containing Receptors.International journal of molecular sciences · 2020Article
- Regenerative Adaptation to Electrochemical Perturbation in Planaria: A Molecular Analysis of Physiological Plasticity.iScience · 2019Article
- Oxygen-Glucose Deprivation Differentially Affects Neocortical Pyramidal Neurons and Parvalbumin-Positive Interneurons.Neuroscience · 2019Article
- Role of UCHL1 in axonal injury and functional recovery after cerebral ischemia.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- The weak voltage dependence of pannexin 1 channels can be tuned by N-terminal modifications.The Journal of general physiology · 2018Article
- Therapeutic strategies targeting connexins.Nature reviews. Drug discovery · 2018Review
- N-Glycosylation Regulates Pannexin 2 Localization but Is Not Required for Interacting with Pannexin 1.International journal of molecular sciences · 2018Article
- Role of glial-like type II cells as paracrine modulators of carotid body chemoreception.Physiological genomics · 2018Article
- Targeting NMDA receptors in stroke: new hope in neuroprotection.Molecular brain · 2018Review
- Trovafloxacin attenuates neuroinflammation and improves outcome after traumatic brain injury in mice.Journal of neuroinflammation · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An ischaemic stroke occurs during loss of blood flow in the brain from the occlusion of a blood vessel. The ischaemia itself comprises a complex array of insults, including oxygen and glucose deprivation (OGD), glutamate excitotoxicity, acidification/hypercapnia, and loss of sheer forces. A substantial amount of knowledge has accumulated that define the excitotoxic cascade downstream of N-methyl-d-aspartate receptors (NMDARs). While the NMDAR can influence numerous downstream elements, one critical target during ischaemia is the ion channel, pannexin-1 (Panx1). The C-terminal region of Panx1 appears critical for its regulation under a host of physiological and pathological stimuli. We have shown using hippocampal brain slices that Panx1 is activated by NMDARs through Src family kinases. However, it is not yet certain if this involves direct phosphorylation of Panx1 or an allosteric interaction between the channel's C-terminal tail and Src. Interestingly, Panx1 opening during ischaemia and NMDAR over-activation is antagonized by an interfering peptide that comprises amino acids 305-318 of Panx1. Thus, targeting the activation of Panx1 by NMDARs and Src kinases is an attractive mechanism to reduce anoxic depolarizations and neuronal death.
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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.