ArticleChannels (Austin, Tex.)2017
TRPM4 activation by chemically- and oxygen deprivation-induced ischemia and reperfusion triggers neuronal death.
Article in Channels (Austin, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Necrosis by sodium overload: a potential mechanism for renal diseases associated with mitochondrial dysfunction.Cell death discovery · 2026Article
- Integrative Machine Learning Framework Revealing TRPM4-Associated Signatures and Identifying SPATA6 as a Potential Biomarker in Prostate Cancer.Journal of Cancer · 2026Article
- Protective effect of antidiabetic drugs against male infertility: evidence from Mendelian randomization.Diabetology & metabolic syndrome · 2025Article
- TRP Channels in Excitotoxicity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025Review
- A glibenclamide-sensitive TRPM4-mediated component of CA1 excitatory postsynaptic potentials appears in experimental autoimmune encephalomyelitis.Scientific reports · 2022Article
- Novel oxygen sensing mechanism in the spinal cord involved in cardiorespiratory responses to hypoxia.Science advances · 2022Article
- IInternational journal of molecular sciences · 2021Article
- TRPM4 Expression During Postnatal Developmental of Mouse CA1 Pyramidal Neurons.Frontiers in neuroanatomy · 2021Article
- TRP Channels Regulation of Rho GTPases in Brain Context and Diseases.Frontiers in cell and developmental biology · 2020Review
- TRPM4 and the Emperor.Channels (Austin, Tex.) · 2018Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral ischemia-reperfusion injury triggers a deleterious process ending in neuronal death. This process has two components, a glutamate-dependent and a glutamate-independent mechanism. In the glutamate-independent mechanism, neurons undergo a slow depolarization eventually leading to neuronal death. However, little is known about the molecules that take part in this process. Here we show by using mice cortical neurons in culture and ischemia-reperfusion protocols that TRPM4 is fundamental for the glutamate-independent neuronal damage. Thus, by blocking excitotoxicity, we reveal a slow activating, glibenclamide- and 9-phenanthrol-sensitive current, which is activated within 5 min upon ischemia-reperfusion onset. TRPM4 shRNA-based silenced neurons show a reduced ischemia-reperfusion induced current and depolarization. Neurons were protected from neuronal death up to 3 hours after the ischemia-reperfusion challenge. The activation of TRPM4 during ischemia-reperfusion injury involves the increase in both, intracellular calcium and H
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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.