ReviewNeurogastroenterology and motility2019
Targeting epigenetic mechanisms for chronic visceral pain: A valid approach for the development of novel therapeutics.
Review in Neurogastroenterology and motility, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Mendelian randomization study of gastroesophageal reflux disease and major depression.PloS one · 2023Pooled it
- Overexpression of small-conductance Ca2+-activated K+ channel 2 attenuates pain-like behavior in female mice with cystitis.JCI insight · 2026Article
- Article
- Review
- N4-acetylcytidine acetylation of neurexin 2 in the spinal dorsal horn regulates hypersensitivity in a rat model of cancer-induced bone pain.Molecular therapy. Nucleic acids · 2024Article
- Upregulation of KDM6B in the anterior cingulate cortex contributes to neonatal maternal deprivation-induced chronic visceral pain in mice.Molecular pain · 2024Article
- Research Progress of Central and Peripheral Corticotropin-Releasing Hormone in Irritable Bowel Syndrome with Comorbid Dysthymic Disorders.Gut and liver · 2024Review
- Activation of EphrinB2/EphB2 signaling in the spine cord alters glia-neuron interactions in mice with visceral hyperalgesia following maternal separation.Frontiers in pharmacology · 2024Article
- Gallic Acid Alleviates Visceral Pain and Depression via Inhibition of P2X7 Receptor.International journal of molecular sciences · 2022Article
- Association Between Psychosocial Disorders and Gastroesophageal Reflux Disease: A Systematic Review and Meta-analysis.Journal of neurogastroenterology and motility · 2022Review
- Histone deacetylase inhibitor givinostat attenuates nonalcoholic steatohepatitis and liver fibrosis.Acta pharmacologica Sinica · 2022Article
- Role of hippocampal circKcnk9 in visceral hypersensitivity and anxiety comorbidity of irritable bowel syndrome.Frontiers in cellular neuroscience · 2022Article
- Digital Analgesic Comprising a Second-Generation Digital Health System: Increasing Effectiveness by Optimizing the Dosing and Minimizing Side Effects.Journal of pain research · 2022Review
- Research hotspots and trends in visceral pain research: A global comprehensive bibliometric analysis.Frontiers in molecular neuroscience · 2022Article
- Environmental enrichment prevents stress-induced epigenetic changes in the expression of glucocorticoid receptor and corticotrophin releasing hormone in the central nucleus of the amygdala to inhibit visceral hypersensitivity.Experimental neurology · 2021Article
- Global gene expression and chromatin accessibility of the peripheral nervous system in animal models of persistent pain.Journal of neuroinflammation · 2021Article
- Upregulation of TRPC6 Mediated by PAX6 Hypomethylation Is Involved in the Mechanical Allodynia Induced by Chemotherapeutics in Dorsal Root Ganglion.The international journal of neuropsychopharmacology · 2020Article
- Altered BDNF Methylation in Patients with Chronic Musculoskeletal Pain and High Biopsychosocial Complexity.Journal of pain research · 2020Article
- Differential DNA methylation in Black and White individuals with chronic low back pain enrich different genomic pathways.Neurobiology of pain (Cambridge, Mass.)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChronic visceral pain is persistent pain emanating from thoracic, pelvic, or abdominal origin that is poorly localized with regard to the specific organ affected. The prevalence can range up to 25% in the adult population as chronic visceral pain is a common feature of many visceral disorders, which may or may not be accompanied by distinct structural or histological abnormalities within the visceral organs. Mounting evidence suggests that changes in epigenetic mechanisms are involved in the top-down or bottom-up sensitization of pain pathways and the development of chronic pain. Epigenetic changes can lead to long-term alterations in gene expression profiles of neurons and consequently alter functionality of peripheral neurons, dorsal root ganglia, spinal cord, and brain neurons. However, epigenetic modifications are dynamic, and thus, detrimental changes may be reversible. Hence, external factors/therapeutic interventions may be capable of modulating the epigenome and restore normal gene expression for extended periods of time. PURPOSE: The goal of this review is to highlight the latest discoveries made toward understanding the epigenetic mechanisms that are involved in the development or maintenance of chronic visceral pain. Furthermore, this review will provide evidence supporting that targeting these epigenetic mechanisms may represent a novel approach to treat chronic visceral pain.
Indexed as
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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.