ArticleThe Journal of clinical endocrinology and metabolism2014
Elevated peritoneal expression and estrogen regulation of nociceptive ion channels in endometriosis.
Article in The Journal of clinical endocrinology and metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 87 citations in OpenAlex.
- Review
- Article
- The Therapeutic Role of Dienogest in Endometriosis-Associated Pain: From Basics to Clinics.Biomolecules · 2026Review
- From Endometriosis to Lipedema: Toward a Neuroimmune Framework for Pain Amplification in Hormone-Sensitive Disorders.Biomedicines · 2026Review
- Nuclear factor IX promotes endometriosis progression through transcriptional activation of tetraspanin-2.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Endometriosis: new insights and opportunities for relief of symptoms.Biology of reproduction · 2025Review
- The ExPAND Study: A Prospective Association Study into Endometriosis-Associated Pain, Neurosteroid Synthesis, and TRPM3.Biomolecules · 2025Article
- Associations between endogenous sex hormones and multisite chronic musculoskeletal pain.British journal of anaesthesia · 2025Article
- Unveiling the Mechanisms of Pain in Endometriosis: Comprehensive Analysis of Inflammatory Sensitization and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Neuroinflammation is responsible for pain in endometriosis - targeting the JAK-STAT pathway and mast cell activation.Frontiers in immunology · 2025Review
- Unravelling the Intricate Link: Mast Cells and Estrogen-Induced Pain Sensitization in Endometriosis.International journal of biological sciences · 2025Review
- TRPV1 Channel in Human Eosinophils: Functional Expression and Inflammatory Modulation.International journal of molecular sciences · 2024Article
- A Lifelong Impact on Endometriosis: Pathophysiology and Pharmacological Treatment.International journal of molecular sciences · 2023Review
- TRPA1 Role in Inflammatory Disorders: What Is Known So Far?International journal of molecular sciences · 2022Review
- Identification ofPharmacogenomics and personalized medicine · 2022Article
- Eliapixant is a selective P2X3 receptor antagonist for the treatment of disorders associated with hypersensitive nerve fibers.Scientific reports · 2021Article
- The role of peripheral nerve signaling in endometriosis.FASEB bioAdvances · 2021Review
- TRP Channels as Sensors of Aldehyde and Oxidative Stress.Biomolecules · 2021Review
- Role of sex hormones in modulating breast and ovarian cancer associated pain.Molecular and cellular endocrinology · 2021Article
- Tetrodotoxin: A New Strategy to Treat Visceral Pain?Toxins · 2021Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
contextOvarian suppression is a common treatment for endometriosis-associated pelvic pain. Its exact mechanism of action is poorly understood, although it is assumed to reflect reduced production/action of estrogens.
objectiveThe objective of the study was to measure the expression of mRNAs encoded by nociceptive genes in the peritoneum of women with chronic pelvic pain (CPP) with or without endometriosis and to investigate whether estrogens alter nociceptive gene expression in human sensory neurons.
designThe study was performed using human tissue analysis and cell culture.
settingThe study was conducted at a university research institute. PATIENTS: Peritoneal biopsies were obtained from women with CPP and endometriosis (n = 12), CPP and no endometriosis (n = 10), and no pain or endometriosis (n = 5). Endometriosis lesions were obtained from women with endometriosis (n = 18).
main outcome measuresmRNAs encoding ion channels (P2RX3, SCN9A, SCN11A, TRPA1, TRPV1) and the neurotransmitter TAC1 were measured in human tissue samples and in human embryonic stem cell-derived sensory neurons treated with estrogens.
resultsTRPV1, TRPA1, and SCN11A mRNAs were significantly higher in the peritoneum from women with endometriosis (P < .001, P < .01). TRPV1, SCN9A, and TAC1 were elevated in endometriosis lesions (P < .05). P2RX3 mRNA was increased in the peritoneum of women with CPP, with and without endometriosis (P < .05). Incubation of sensory neurons with 17β-estradiol increased TRPV1 mRNA (P < .01). The estrogen receptor-β-selective agonist 2,3-bis(4-hydroxy-phenyl)-propionitrile increased concentrations of TRPV1, P2RX3, SCN9A, and TAC1 mRNAs.
conclusionsEstrogen-dependent expression of TRPV1 in sensory neurons may explain why ovarian suppression can reduce endometriosis-associated pain. Strategies directly targeting ion channels may offer an alternative option for the management of CPP.
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