ReviewCNS & neurological disorders drug targets2012
Janus molecule I: dichotomous effects of COMT in neuropathic vs nociceptive pain modalities.
Review in CNS & neurological disorders drug targets, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 36 citations in OpenAlex.
- Biopsychosocial influence on shoulder pain: Rationale and protocol for a pre-clinical trial.Contemporary clinical trials · 2017Trial
- COMT and MTHFR Genetic Variants Combined Effects on Adolescent Idiopathic Scoliosis Progression.Journal of genomics · 2025Article
- Neurobiology of bruxism: The impact of stress (Review).Biomedical reports · 2024Review
- Nutrient insufficiencies and deficiencies involved in the pathogenesis of bruxism (Review).Experimental and therapeutic medicine · 2023Review
- Evidence Regarding Pharmacogenetics in Pain Management and Cancer.The oncologist · 2023Article
- Evaluation of Analgesic and Anti-inflammatory Activities of Methanolic Leaf and Root Extracts ofJournal of experimental pharmacology · 2023Article
- Plasma Concentrations of Select Inflammatory Cytokines Predicts Pain Intensity 48 Hours Post-Shoulder Muscle Injury.The Clinical journal of pain · 2020Article
- Contribution of COMT and BDNF Genotype and Expression to the Risk of Transition From Acute to Chronic Low Back Pain.The Clinical journal of pain · 2020Article
- Systems pharmacogenomics - gene, disease, drug and placebo interactions: a case study in COMT.Pharmacogenomics · 2019Article
- Overexpression of P2X3 and P2X7 Receptors and TRPV1 Channels in Adrenomedullary Chromaffin Cells in a Rat Model of Neuropathic Pain.International journal of molecular sciences · 2019Article
- Combining Human and Rodent Genetics to Identify New Analgesics.Neuroscience bulletin · 2018Review
- Association between theBalkan journal of medical genetics : BJMG · 2015Article
- COMT gene locus: new functional variants.Pain · 2015Article
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- Chronic pain after lower abdominal surgery: do catechol-O-methyl transferase/opioid receptor μ-1 polymorphisms contribute?Molecular pain · 2013Article
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
Abstract
The enzyme catechol-O-methyltransferase (COMT) has been shown to play a critical role in pain perception by regulating levels of epinephrine (Epi) and norepinephrine (NE). Although the key contribution of catecholamines to the perception of pain has been recognized for a long time, there is a clear dichotomy of observations. More than a century of research has demonstrated that increasing adrenergic transmission in the spinal cord decreases pain sensitivity in animals. Equally abundant evidence demonstrates the opposite effect of adrenergic signaling in the peripheral nervous system, where adrenergic signaling increases pain sensitivity. Viewing pain processing within spinal and peripheral compartments and determining the directionality of adrenergic signaling helps clarify the seemingly contradictory findings of the pain modulatory properties of adrenergic receptor agonists and antagonists presented in other reviews. Available evidence suggests that adrenergic signaling contributes to pain phenotypes through α(1/2) and β(2/3) receptors. While stimulation of α(2) adrenergic receptors seems to uniformly produce analgesia, stimulation of α(1) or β receptors produces either analgesic or hyperalgesic effects. Establishing the directionality of adrenergic receptor modulation of pain processing, and related COMT activity in different pain models are needed to bring meaning to recent human molecular genetic findings. This will enable the translation of current findings into meaningful clinical applications such as diagnostic markers and novel therapeutic targets for complex human pain conditions.
Indexed as
Identifiers
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.