ReviewCNS neuroscience & therapeutics2025
Transient Receptor Potential Channels as Key Regulators of Neuroinflammation in Neurological Disorders: Mechanistic Insights, Therapeutic Potentials, and Future Directions.
Review in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- TRPC6-Mediated CaCells · 2026Article
- Molecular mechanisms of perimenopausal cognitive impairment in a rat model: multi-omics integration reveals the Adgrl2-Camk2d-TRPV1 signaling axis mediating calcium homeostasis disruption and neuroinflammation.Frontiers in aging neuroscience · 2026Article
- Transient Receptor Potential Channels as Key Regulators of Neuroinflammation in Neurological Disorders: Mechanistic Insights, Therapeutic Potentials, and Future Directions.CNS neuroscience & therapeutics · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
backgroundTransient receptor potential (TRP) ion channels, a ubiquitous family of nonselective cation channels, are extensively expressed across the nervous system, immune system, and peripheral tissues. These channels serve as critical sensors for detecting temperature, mechanical forces, and chemical stimuli, thereby regulating numerous physiological and pathological processes. Over the past decade, their pivotal role in neuroimmune crosstalk and inflammatory signaling has emerged as a key focus within neuroscience research.
methodsA comprehensive literature review was conducted in PubMed using key terms "TRP channel," "neuroinflammation," and each of the following neurological disorders: neuropathic pain, migraine, stroke, multiple sclerosis (MS), Alzheimer's disease (AD), Parkinson's disease (PD), autism spectrum disorder (ASD), epilepsy, and psychiatric disorders.
resultsThis review synthesizes the current evidence to elucidate the dual-edged contributions of TRP channels as mediators of inflammation in neuropathic pain, migraine, stroke, MS, AD, PD, ASD, epilepsy, and psychiatric disorders. Furthermore, we also evaluate emerging therapeutic strategies targeting TRP channels, encompassing both nonpharmacological approaches and pharmacological interventions.
conclusionsBy integrating mechanistic insights with translational perspectives, this review highlights TRP channels as promising targets for precision medicine and underscores their potential in the development of novel, mechanism-based therapies for complex neurological disorders, thereby advancing a new era of targeted neuroimmunomodulation.
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What Socratic 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 Socratic graph.