ArticleMolecular neurobiology2017
TRPC3/6/7 Knockdown Protects the Brain from Cerebral Ischemia Injury via Astrocyte Apoptosis Inhibition and Effects on NF-кB Translocation.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 47 citations in OpenAlex.
- Pathological mechanisms and therapeutic potential of MSC-Exos in ischemic stroke management.Stem cell research & therapy · 2026Review
- Neuroprotective Delivery of Dexmedetomidine Liposomes Mitigates Cerebral Energy Crisis by Modulating Calcium-Driven Aerobic Glycolysis in Cerebral Ischemia-Reperfusion Injury.International journal of nanomedicine · 2026Article
- Transient Receptor Potential Channels as Key Regulators of Neuroinflammation in Neurological Disorders: Mechanistic Insights, Therapeutic Potentials, and Future Directions.CNS neuroscience & therapeutics · 2025Review
- TRPC Channels Activated by G Protein-Coupled Receptors Drive CaTranslational stroke research · 2024Article
- TRP Channels in Stroke.Neuroscience bulletin · 2024Review
- The mechanosensitive ion channel Piezo1 modulates the migration and immune response of microglia.iScience · 2023Article
- Transient receptor potential ion channels and cerebral stroke.Brain and behavior · 2023Review
- Role of TRP ion channels in cerebral circulation and neurovascular communication.Neuroscience letters · 2021Review
- Heteromeric TRP Channels in Lung Inflammation.Cells · 2021Review
- Novel Mechanistic Insights and Potential Therapeutic Impact of TRPC6 in Neurovascular Coupling and Ischemic Stroke.International journal of molecular sciences · 2021Review
- The Role of TRPC6 in Renal Ischemia/Reperfusion and Cellular Hypoxia/Reoxygenation Injuries.Frontiers in molecular biosciences · 2021Article
- Review
- Review
- TRPC6 Attenuates Cortical Astrocytic Apoptosis and Inflammation in Cerebral Ischemic/Reperfusion Injury.Frontiers in cell and developmental biology · 2020Article
- Novel Targets for Stroke Therapy: Special Focus on TRPC Channels and TRPC6.Frontiers in aging neuroscience · 2020Review
- Ischemia-Triggered Glutamate Excitotoxicity From the Perspective of Glial Cells.Frontiers in cellular neuroscience · 2020Article
- Bakuchiol Attenuates Oxidative Stress and Neuron Damage by Regulating Trx1/TXNIP and the Phosphorylation of AMPK After Subarachnoid Hemorrhage in Mice.Frontiers in pharmacology · 2020Article
- Exosomes Secreted From Bone Marrow Mesenchymal Stem Cells Attenuate Oxygen-Glucose Deprivation/Reoxygenation-Induced Pyroptosis in PC12 Cells by Promoting AMPK-Dependent Autophagic Flux.Frontiers in cellular neuroscience · 2020Article
- TRP Channels Regulation of Rho GTPases in Brain Context and Diseases.Frontiers in cell and developmental biology · 2020Review
- Contribution of TRPC Channels in Neuronal Excitotoxicity Associated With Neurodegenerative Disease and Ischemic Stroke.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
Abstract
Ischemia contributes significantly to morbidity and mortality associated with many common neurological diseases. Calcium overload is an important mechanism of cerebral ischemia and reperfusion (I/R) injury. Despite decades of intense research, an effective beneficial treatment of stroke remains limited; few therapeutic strategies exist to combat the consequences of cerebral ischemia. Traditionally, a "neurocentric" view has dominated research in this field. Evidence is now accumulating that glial cells, especially astrocytes, play an important role in the pathophysiology of cerebral ischemia. Here, we show that transient receptor potential (TRP)C3/6/7 knockout (KO) mice subjected to an I/R procedure demonstrate ameliorated brain injury (infract size), compared to wild-type (WT) control animals. This is accompanied by reduction of NF-кB phosphorylation and an increase in protein kinase B (AKT) phosphorylation in I/R-injured brain tissues in TRPC3/6/7 KO mice. Also, the expression of pro-apoptotic protein Bcl-2 associated X (Bax) is down-regulated and that of anti-apoptotic protein Bcl-2 is upregulated in TRPC3/6/7
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What OpenQuestion holds
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.