ReviewBiochimica et biophysica acta2007
Non-selective cation channels, transient receptor potential channels and ischemic stroke.
Review in Biochimica et biophysica acta, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
32 citing papers in PubMed, 77 citations in OpenAlex.
- Review
- TRPM4 Blocking Antibody Protects Cerebral Vasculature in Delayed Stroke Reperfusion.Biomedicines · 2023Article
- Inhibition of intracellular proton-sensitive CaActa pharmaceutica Sinica. B · 2022Article
- Pharmacological Modulation and (Patho)Physiological Roles of TRPM4 Channel-Part 2: TRPM4 in Health and Disease.Pharmaceuticals (Basel, Switzerland) · 2021Review
- A Novel Model for Studying Voltage-Gated Ion Channel Gene Expression during Reversible Ischemic Stroke.International journal of medical sciences · 2019Article
- SUR1-TRPM4 channel activation and phasic secretion of MMP-9 induced by tPA in brain endothelial cells.PloS one · 2018Article
- Mitochondrial Mechanisms of Neuronal Cell Death: Potential Therapeutics.Annual review of pharmacology and toxicology · 2017Review
- Article
- The fate of medications evaluated for ischemic stroke pharmacotherapy over the period 1995-2015.Acta pharmaceutica Sinica. B · 2016Review
- Detrimental or beneficial: the role of TRPM2 in ischemia/reperfusion injury.Acta pharmacologica Sinica · 2016Review
- Ischemic optic neuropathies and their models: disease comparisons, model strengths and weaknesses.Japanese journal of ophthalmology · 2015Review
- TRP Channels in Respiratory Pathophysiology: the Role of Oxidative, Chemical Irritant and Temperature Stimuli.Current neuropharmacology · 2015Review
- TRPM4 inhibition promotes angiogenesis after ischemic stroke.Pflugers Archiv : European journal of physiology · 2014Article
- Disruption of ion homeostasis in the neurogliovascular unit underlies the pathogenesis of ischemic cerebral edema.Translational stroke research · 2014Review
- Ionotropic receptors and ion channels in ischemic neuronal death and dysfunction.Acta pharmacologica Sinica · 2013Review
- TRPM2 channel activation following in vitro ischemia contributes to male hippocampal cell death.Neuroscience letters · 2012Article
- Ginsenoside-Rd attenuates TRPM7 and ASIC1a but promotes ASIC2a expression in rats after focal cerebral ischemia.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2012Article
- Sulfonylurea receptor 1 in central nervous system injury: a focused review.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2012Review
- On potential interactions between non-selective cation channel TRPM4 and sulfonylurea receptor SUR1.The Journal of biological chemistry · 2012Article
- Comparative effects of glibenclamide and riluzole in a rat model of severe cervical spinal cord injury.Experimental neurology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Several pathways to neural cell death are involved in ischemic stroke, and all require monovalent or divalent cation influx, implicating non-selective cation (NC) channels. NC channels are also likely to be involved in the dysfunction of vascular endothelial cells that leads to formation of edema following cerebral ischemia. Two newly described NC channels have emerged as potential participants in ischemic stroke, the acid sensing ion channel (ASIC), and the sulfonylurea receptor-1 (SUR1)-regulated NC(Ca-ATP) channel. Non-specific blockers of NC channels, including pinokalant (LOE 908 MS) and rimonabant (SR141716A), have beneficial effects in rodent models of ischemic stroke. Evidence is accumulating that NC channels formed by members of the transient receptor potential (TRP) family are also up-regulated in ischemic stroke and may play a direct role in calcium-mediated neuronal death. The nascent field of NC channels, including TRP channels, in ischemic stroke is poised to provide novel mechanistic insights and therapeutic strategies for this often devastating human condition.
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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.