ReviewCurrent neuropharmacology2020
Selenium and Neurological Diseases: Focus on Peripheral Pain and TRP Channels.
Review in Current neuropharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
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.
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Who cites it
37 citing papers in PubMed, 85 citations in OpenAlex.
- TRPA1 Channels as Multimodal Environmental Sensors: Structure-Function Insights From Aquatic Organisms.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Selenium-Loaded Calcium Phosphate with Long-Term and Curative Dosage Drug Release for Post-Surgical Osteosarcoma Management and Osteogenesis.International journal of molecular sciences · 2026Article
- Protective effects of zingerone against bisphenol-A induced oxidative stress and apoptosis in SH-SY5Y cells: the role of TRPM2 channel.Molecular biology reports · 2026Article
- Vitamin E Intake Modulates the Effect of Selenomethionine on Sexual Function and Depressive Symptoms in Reproductive-Age Women with Euthyroid Autoimmune Thyroiditis: A Pilot Study.Antioxidants (Basel, Switzerland) · 2026Article
- Nutritional selenium status in a cohort of university students: impact on intellectual and cognitive performance.Frontiers in nutrition · 2026Article
- Protective potential of tween 80-functionalized chitosan-selenium nanoparticles containing quercetin against cisplatin neurotoxicity in PC12 cells: an in vitro and network pharmacology study.Scientific reports · 2025Article
- Article
- Bridging systemic metabolic dysfunction and Alzheimer's disease: the liver interface.Molecular neurodegeneration · 2025Review
- Curcumin protects against MPPMolecular biology reports · 2025Article
- The Effect of Selenium Against Cadmium-Induced Nephrotoxicity in Rats: The Role of the TRPM2 Channel.Toxics · 2025Article
- Mesenchymal stem cells as a therapeutic strategy to combat oxidative stress-mediated neuropathic pain.BioImpacts : BI · 2025Review
- The chondrocyte "mechanome": Activation of the mechanosensitive ion channels TRPV4 and PIEZO1 drives unique transcriptional signatures.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- The role of TRPV4 in programmed cell deaths.Molecular biology reports · 2024Review
- Analysis of Ionomic Profiles of Spinal Cords in a Rat Model with Bone Cancer Pain.Journal of pain research · 2024Article
- Characterization and anti-inflammatory effect of selenium-enriched probiotic Bacillus amyloliquefaciens C-1, a potential postbiotics.Scientific reports · 2023Article
- Involvement of TRPM2 Channel on Doxorubicin-Induced Experimental Cardiotoxicity Model: Protective Role of Selenium.Biological trace element research · 2023Article
- Involvement of TRPM7 Channel on the Induction of Diabetic Neuropathic Pain in Mice: Protective Role of Selenium and Curcumin.Biological trace element research · 2023Article
- Association between selenium intake and migraine: a nationwide cross-sectional study.Frontiers in neuroscience · 2023Article
- TRPV1 stimulation increased oxidative neurotoxicity and apoptosis in the glia cell membrane but not in the perinuclear area: An evidence of TRPV1 subtype.Metabolic brain disease · 2022Article
- Small molecule compound M12 reduces vascular permeability in obese mice via blocking endothelial TRPV4-Nox2 interaction.Acta pharmacologica Sinica · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pain is a complex physiological process that includes many components. Growing evidence supports the idea that oxidative stress and Ca2+ signaling pathways participate in pain detection by neurons. The main source of endogenous reactive oxygen species (ROS) is mitochondrial dysfunction induced by membrane depolarization, which is in turn caused by Ca2+ influx into the cytosol of neurons. ROS are controlled by antioxidants, including selenium. Selenium plays an important role in the nervous system, including the brain, where it acts as a cofactor for glutathione peroxidase and is incorporated into selenoproteins involved in antioxidant defenses. It has neuroprotective effects through modulation of excessive ROS production, inflammation, and Ca2+ overload in several diseases, including inflammatory pain, hypersensitivity, allodynia, diabetic neuropathic pain, and nociceptive pain. Ca2+ entry across membranes is mediated by different channels, including transient receptor potential (TRP) channels, some of which (e.g., TRPA1, TRPM2, TRPV1, and TRPV4) can be activated by oxidative stress and have a role in the induction of peripheral pain. The results of recent studies indicate the modulator roles of selenium in peripheral pain through inhibition of TRP channels in the dorsal root ganglia of experimental animals. This review summarizes the protective role of selenium in TRP channel regulation, Ca2+ signaling, apoptosis, and mitochondrial oxidative stress in peripheral pain induction.
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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.