ReviewActa pharmacologica Sinica2013
Ionotropic receptors and ion channels in ischemic neuronal death and dysfunction.
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 40 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
40 citing papers in PubMed, 83 citations in OpenAlex.
- Ion Channels and Neurological Disease-2nd Edition.Life (Basel, Switzerland) · 2026Article
- Neurochemical Mechanisms Underlying Tanshinone-Mediated Neuroprotection and Formulation Strategies in Cerebral Ischemia/Reperfusion Injury.Neurochemical research · 2026Review
- New advances in small molecule drugs targeting NMDA receptors.Acta pharmacologica Sinica · 2026Review
- Immediate Consequences of a Spinal Cord Injury During Development: Unique Insights From Ex Vivo Models.Neural plasticity · 2026Review
- Differential Protective Effects of Edaravone in Cerebellar and Hippocampal Ischemic Injury Models.Cerebellum (London, England) · 2025Article
- Advancements in Targeting Ion Channels for the Treatment of Neurodegenerative Diseases.Pharmaceuticals (Basel, Switzerland) · 2024Review
- The SWELL1 Channel Promotes Ischemic Brain Damage by Mediating Neuronal Swelling and Glutamate Toxicity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Causal relations between ischemic stroke and epilepsy: A bidirectional Mendelian randomization study.Heliyon · 2024Article
- Pannexin-1 opening in neuronal edema causes cell death but also leads to protection via increased microglia contacts.Cell reports · 2023Article
- Advances in Therapies to Treat Neonatal Hypoxic-Ischemic Encephalopathy.Journal of clinical medicine · 2023Review
- The Oxygen and Glucose Deprivation of Immature Cells of the Nervous System Exerts Distinct Effects on Mitochondria, Mitophagy, and Autophagy, Depending on the Cells' Differentiation Stage.Brain sciences · 2023Article
- Article
- Excitatory Synaptic Transmission in Ischemic Stroke: A New Outlet for Classical Neuroprotective Strategies.International journal of molecular sciences · 2022Review
- CXCL13 expressed on inflamed cerebral blood vessels recruit IL-21 producing TJournal of neuroinflammation · 2022Article
- From kitchen to clinic: Pharmacotherapeutic potential of common spices in Indian cooking in age-related neurological disorders.Frontiers in pharmacology · 2022Review
- Convergent NMDA receptor-Pannexin1 signaling pathways regulate the interaction of CaMKII with Connexin-36.Communications biology · 2021Article
- Mast Cell and Astrocyte Hemichannels and Their Role in Alzheimer's Disease, ALS, and Harmful Stress Conditions.International journal of molecular sciences · 2021Review
- Astaxanthin Counteracts Excitotoxicity and Reduces the Ensuing Increases in Calcium Levels and Mitochondrial Reactive Oxygen Species Generation.Marine drugs · 2020Article
- Persistent Neurovascular Unit Dysfunction: Pathophysiological Substrate and Trigger for Late-Onset Neurodegeneration After Traumatic Brain Injury.Frontiers in neuroscience · 2020Article
- Therapeutic Effect of Agmatine on Neurological Disease: Focus on Ion Channels and Receptors.Neurochemical research · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Loss of energy supply to neurons during stroke induces a rapid loss of membrane potential that is called the anoxic depolarization. Anoxic depolarizations result in tremendous physiological stress on the neurons because of the dysregulation of ionic fluxes and the loss of ATP to drive ion pumps that maintain electrochemical gradients. In this review, we present an overview of some of the ionotropic receptors and ion channels that are thought to contribute to the anoxic depolarization of neurons and subsequently, to cell death. The ionotropic receptors for glutamate and ATP that function as ligand-gated cation channels are critical in the death and dysfunction of neurons. Interestingly, two of these receptors (P2X7 and NMDAR) have been shown to couple to the pannexin-1 (Panx1) ion channel. We also discuss the important roles of transient receptor potential (TRP) channels and acid-sensing ion channels (ASICs) in responses to ischemia. The central challenge that emerges from our current understanding of the anoxic depolarization is the need to elucidate the mechanistic and temporal interrelations of these ion channels to fully appreciate their impact on neurons during 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.