ArticleJournal of neurogastroenterology and motility2015
Role of Corticotropin-releasing Factor Signaling in Stress-related Alterations of Colonic Motility and Hyperalgesia.
Article in Journal of neurogastroenterology and motility, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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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.
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Who cites it
49 citing papers in PubMed, 96 citations in OpenAlex.
- Antagonizing the corticotropin-releasing hormone receptor 1 with an orally bioavailable drug reduces endometriosis pain and associated adhesions†.Biology of reproduction · 2026Article
- Protective Effect of Uric Acid on Rat Model of Irritable Bowel Syndrome Requires Brain-Gut Communication Through Vagal Cholinergic Pathways.Neurogastroenterology and motility · 2026Article
- Quercetin and Tranylcypromine Improve Memory, Behavioral Performance, and Cholinergic Function in Male Rats Subjected to Chronic Restraint Stress.Brain sciences · 2025Article
- Electroconvulsive therapy improves distal colonic motility via the subdiaphragmatic vagus nerve in depressive-like mice.Scientific reports · 2025Article
- Pharmacogenetics in IBS: update and impact of GWAS studies in drug targets and metabolism.Expert opinion on drug metabolism & toxicology · 2024Review
- Toll-like receptor 4 plays a vital role in irritable bowel syndrome: a scoping review.Frontiers in immunology · 2024Article
- Connecting dots in disorders of gut-brain interaction: the interplay of stress and sex hormones in shaping visceral pain.Frontiers in psychiatry · 2023Review
- Genetics of irritable bowel syndrome: shifting gear via biobank-scale studies.Nature reviews. Gastroenterology & hepatology · 2022Review
- Article
- Mast cell mediation of visceral sensation and permeability in irritable bowel syndrome.Neurogastroenterology and motility · 2022Review
- Pathophysiological Commonality Between Irritable Bowel Syndrome and Metabolic Syndrome: Role of Corticotropin-releasing Factor-Toll-like Receptor 4-Proinflammatory Cytokine Signaling.Journal of neurogastroenterology and motility · 2022Review
- Supraspinal Mechanisms of Intestinal Hypersensitivity.Cellular and molecular neurobiology · 2022Review
- Chronic restraint stress produces sex-specific behavioral and molecular outcomes in the dorsal and ventral rat hippocampus.Neurobiology of stress · 2022Article
- Potential Mechanisms of Acupuncture for Functional Dyspepsia Based on Pathophysiology.Frontiers in neuroscience · 2021Review
- CRF serum levels differentiate PTSD from healthy controls and TBI in military veterans.Psychiatric research and clinical practice · 2021Article
- Optimizing Autonomic Function Analysis via Heart Rate Variability Associated With Motor Activity of the Human Colon.Frontiers in physiology · 2021Article
- Overexpression of corticotropin-releasing factor in intestinal mucosal eosinophils is associated with clinical severity in Diarrhea-Predominant Irritable Bowel Syndrome.Scientific reports · 2020Article
- Peripheral mechanisms contribute to comorbid visceral hypersensitivity induced by preexisting orofacial pain and stress in female rats.Neurogastroenterology and motility · 2020Article
- Review
- Epigenetic Mechanisms in Irritable Bowel Syndrome.Frontiers in psychiatry · 2020Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The corticotropin-releasing factor (CRF) signaling systems encompass CRF and the structurally related peptide urocortin (Ucn) 1, 2, and 3 along with 2 G-protein coupled receptors, CRF₁ and CRF₂. CRF binds with high and moderate affinity to CRF₁ and CRF₂ receptors, respectively while Ucn1 is a high-affinity agonist at both receptors, and Ucn2 and Ucn3 are selective CRF₂ agonists. The CRF systems are expressed in both the brain and the colon at the gene and protein levels. Experimental studies established that the activation of CRF₁ pathway in the brain or the colon recaptures cardinal features of diarrhea predominant irritable bowel syndrome (IBS) (stimulation of colonic motility, activation of mast cells and serotonin, defecation/watery diarrhea, and visceral hyperalgesia). Conversely, selective CRF1 antagonists or CRF₁/CRF₂ antagonists, abolished or reduced exogenous CRF and stress-induced stimulation of colonic motility, defecation, diarrhea and colonic mast cell activation and visceral hyperalgesia to colorectal distention. By contrast, the CRF₂ signaling in the colon dampened the CRF₁ mediated stimulation of colonic motor function and visceral hyperalgesia. These data provide a conceptual framework that sustained activation of the CRF₁ system at central and/or peripheral sites may be one of the underlying basis of IBS-diarrhea symptoms. While targeting these mechanisms by CRF₁ antagonists provided a relevant novel therapeutic venue, so far these promising preclinical data have not translated into therapeutic use of CRF₁ antagonists. Whether the existing or newly developed CRF₁ antagonists will progress to therapeutic benefits for stress-sensitive diseases including IBS for a subset of patients is still a work in progress.
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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.