ArticleJournal of spine2013
The Sur1-Trpm4 Channel in Spinal Cord Injury.
Article in Journal of spine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Quantifying injury expansion in the cervical spinal cord with intravital ultrafast contrast-enhanced ultrasound imaging.Experimental neurology · 2024Article
- A glibenclamide-sensitive TRPM4-mediated component of CA1 excitatory postsynaptic potentials appears in experimental autoimmune encephalomyelitis.Scientific reports · 2022Article
- Hemorrhage and Locomotor Deficits Induced by Pain Input after Spinal Cord Injury Are Partially Mediated by Changes in Hemodynamics.Journal of neurotrauma · 2021Article
- Sulfonylurea Receptor 1 in Central Nervous System Injury: An Updated Review.International journal of molecular sciences · 2021Review
- Glibenclamide Treatment in Traumatic Brain Injury: Operation Brain Trauma Therapy.Journal of neurotrauma · 2021Article
- Contribution of Brain Processes to Tissue Loss After Spinal Cord Injury: Does a Pain-Induced Rise in Blood Pressure Fuel Hemorrhage?Frontiers in systems neuroscience · 2021Article
- Pharmacological Transection of Brain-Spinal Cord Communication Blocks Pain-Induced Hemorrhage and Locomotor Deficits after Spinal Cord Injury in Rats.Journal of neurotrauma · 2020Article
- Learning to promote recovery after spinal cord injury.Experimental neurology · 2020Review
- A brief period of moderate noxious stimulation induces hemorrhage and impairs locomotor recovery after spinal cord injury.Physiology & behavior · 2019Article
- Short-term inhibition of fibrinolytic system restores locomotor function after spinal cord injury in mice.Scientific reports · 2019Article
- Matrix metalloproteinase signals following neurotrauma are right on cue.Cellular and molecular life sciences : CMLS · 2019Review
- Sulfonylurea Receptor 1, Transient Receptor Potential Cation Channel Subfamily M Member 4, and KIR6.2:Role in Hemorrhagic Progression of Contusion.Journal of neurotrauma · 2019Article
- Brain-Dependent Processes Fuel Pain-Induced Hemorrhage After Spinal Cord Injury.Frontiers in systems neuroscience · 2019Article
- Engaging pain fibers after a spinal cord injury fosters hemorrhage and expands the area of secondary injury.Experimental neurology · 2019Article
- Hypothermic treatment after computer-controlled compression in minipig: A preliminary report on the effect of epidural vs. direct spinal cord cooling.Experimental and therapeutic medicine · 2018Article
- Involvement of TRPM4 in detrusor overactivity following spinal cord transection in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2018Article
- The ion channel TRPM4 in murine experimental autoimmune encephalomyelitis and in a model of glutamate-induced neuronal degeneration.Molecular brain · 2018Article
- Article
- Endothelin-1 Immunoreactivity and its Association with Intramedullary Hemorrhage and Myelomalacia in Naturally Occurring Disk Extrusion in Dogs.Journal of veterinary internal medicine · 2016Article
- The Sur1-Trpm4 channel regulates NOS2 transcription in TLR4-activated microglia.Journal of neuroinflammation · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Spinal cord injury (SCI) is a major unsolved challenge in medicine. Impact trauma to the spinal cord shears blood vessels, causing an immediate 'primary hemorrhage'. During the hours following trauma, the region of hemorrhage enlarges progressively, with delayed or 'secondary hemorrhage' adding to the primary hemorrhage, and effectively doubling its volume. The process responsible for the secondary hemorrhage that results in early expansion of the hemorrhagic lesion is termed 'progressive hemorrhagic necrosis' (PHN). PHN is a dynamic process of auto destruction whose molecular underpinnings are only now beginning to be elucidated. PHN results from the delayed, progressive, catastrophic failure of the structural integrity of capillaries. The resulting 'capillary fragmentation' is a unique, pathognomonic feature of PHN. Recent work has implicated the Sur1-Trpm4 channel that is newly upregulated in penumbral microvessels as being required for the development of PHN. Targeting the Sur1-Trpm4 channel by gene deletion, gene suppression, or pharmacological inhibition of either of the two channel subunits, Sur1 or Trpm4, yields exactly the same effects histologically and functionally, and exactly the same unique, pathognomonic phenotype - the prevention of capillary fragmentation. The potential advantage of inhibiting Sur1-Trpm4 channels using glibenclamide is a highly promising strategy for ameliorating the devastating sequelae of spinal cord trauma in humans.
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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.