ArticleFrontiers in pharmacology2023
REV-ERB activation as a novel pharmacological approach for treating inflammatory pain.
Article in Frontiers in pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 13 citations in OpenAlex.
- Nociceptor circadian clock genes control excitability and pain perception in mice in a sex- and time-dependent manner.Nature communications · 2026Article
- Perillaldehyde reduces mitochondrial oxidative stress damage by regulating KCNT2/NR1D1 protein activity in vascular dementia rats.Molecular biology reports · 2026Article
- REV-ERBs as regulators of circadian rhythm, neuroinflammation, and glial lipid homeostasis in Alzheimer's disease. A narrative review.British journal of biomedical science · 2026Review
- Modulation of TH17 cell activity by REV-ERB agonists: path toward novel treatments for canine meningoencephalitis of unknown origin.npj veterinary sciences · 2026Review
- Circadian clock and its effect on aging and lifespan.Biogerontology · 2025Review
- Circadian Rhythms and Pain: A Narrative Review on Clock Genes and Circadian-Based Interventions.Journal of pain research · 2025Review
- Mechanism of antagonist ligand binding to REV-ERBα.Scientific reports · 2024Article
- Molecular mechanisms of artificial light at night affecting circadian rhythm disturbance.Archives of toxicology · 2024Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Pain is a complex problem affecting millions of people worldwide. The current therapies to reduce pain are limited as many treatment options inadequately address the causes of pain, lead to tolerance of the drug, or have adverse effects including abuse potential. While there are many causes of pain, one underlying mechanism to the pathogenesis and maintenance of pain conditions is chronic inflammation driven by the NLRP3 inflammasome. Several inflammasome inhibitors are currently under investigation however have the potential to suppress the functioning of the innate immune system, which may cause unwanted affects in patients. Here, we show that the nuclear receptor REV-ERB can suppress the activation of the inflammasome when pharmacologically activated with small molecule agonists. Additionally, REV-ERB activation appears to have analgesic potential in a model of acute inflammatory pain, likely as a result of inflammasome suppression.
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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.