ArticleJournal of neuropathology and experimental neurology2015
Sur1-Trpm4 Cation Channel Expression in Human Cerebral Infarcts.
Article in Journal of neuropathology and experimental neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Neuroprotective effect of Glibenclamide in stroke: a systematic review and meta-analysis of randomized controlled trials.Acta neurologica Belgica · 2026Pooled it
- Efficacy and Safety of Early Treatment with Glibenclamide in Patients with Aneurysmal Subarachnoid Hemorrhage: A Randomized Controlled Trial.Neurocritical care · 2024Trial
- Trial
- Therapeutic potential of alpha-tocopherol in reducing oxidative stress and inflammatory damage after experimental traumatic brain injury and pentylenetetrazol-induced seizures.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- SUR1-TRPM4 is expressed in human epilepsy and promotes neuron hyperactivity and seizures in rodents.Brain : a journal of neurology · 2026Article
- Structural biology of the TRPM4 channel: architecture, modulation, and therapeutic opportunities.Frontiers in pharmacology · 2026Review
- Inhibition of SUR1-TRPM4 attenuates astrocyte swelling and reactivity under oxygen-glucose deprivation/reoxygenation.PloS one · 2026Article
- Article
- Impact of glibenclamide pretreatment on outcomes in acute ischemic stroke patients with type 2 diabetes: a retrospective case-control study.Scientific reports · 2025Article
- RELATIONSHIP BETWEEN TRPM4 RS8104571 GENOTYPE, CIRCULATING TRPM4 AND SUR1, AND CLINICAL OUTCOME FOLLOWING TRAUMATIC BRAIN INJURY.Shock (Augusta, Ga.) · 2025Article
- TRP Channels in Stroke.Neuroscience bulletin · 2024Review
- Dysregulation of Ion Channels and Transporters and Blood-Brain Barrier Dysfunction in Alzheimer's Disease and Vascular Dementia.Aging and disease · 2024Review
- Metabolite transport across central nervous system barriers.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Review
- Alterations in brain fluid physiology during the early stages of development of ischaemic oedema.Fluids and barriers of the CNS · 2024Review
- Resveratrol Prevents Cell Swelling Through Inhibition of SUR1 Expression in Brain Micro Endothelial Cells Subjected to OGD/Recovery.Molecular neurobiology · 2024Article
- Activation of endothelial TRPM2 exacerbates blood-brain barrier degradation in ischemic stroke.Cardiovascular research · 2024Article
- Ion Channel Dysregulation Following Intracerebral Hemorrhage.Neuroscience bulletin · 2024Review
- Novel Activity of Oral Hypoglycemic Agents Linked with Decreased Formation of Tryptophan Metabolite, Kynurenic Acid.Life (Basel, Switzerland) · 2024Article
- New Insights on Mechanisms and Therapeutic Targets of Cerebral Edema.Current neuropharmacology · 2024Review
- Viral protein R (Vpr)-induced neuroinflammation and its potential contribution to neuronal dysfunction: a scoping review.BMC infectious diseases · 2023Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors.
Funding
Abstract
The nonselective monovalent cation channel transient receptor potential melastatin 4 (Trpm4) is transcriptionally upregulated in neural and vascular cells in animal models of brain infarction. It associates with sulfonylurea receptor 1 (Sur1) to form Sur1-Trpm4 channels, which have critical roles in cytotoxic edema, cell death, blood-brain barrier breakdown, and vasogenic edema. We examined Trpm4 expression in postmortem brain specimens from 15 patients who died within the first 31 days of the onset of focal cerebral ischemia. We found increased Trpm4 protein expression in all cases using immunohistochemistry; transcriptional upregulation was confirmed using in situ hybridization of Trpm4 messenger RNA. Transient receptor potential melastatin 4 colocalized and coassociated with Sur1 within ischemic endothelial cells and neurons. Coexpression of Sur1 and Trpm4 in necrotic endothelial cells was also associated with vasogenic edema indicated by upregulated perivascular tumor necrosis factor, extravasation of serum immunoglobulin G, and associated inflammation. Upregulated Trpm4 protein was present up to 1 month after the onset of cerebral ischemia. In a rat model of middle cerebral artery occlusion stroke, pharmacologic channel blockade by glibenclamide, a selective inhibitor of sulfonylurea receptor, mitigated perivascular tumor necrosis factor labeling. Thus, upregulated Sur1-Trpm4 channels and associated blood-brain barrier disruption and cerebral edema suggest that pharmacologic targeting of this channel may represent a promising therapeutic strategy for the clinical management of patients with cerebral ischemia.
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