ReviewReproductive sciences (Thousand Oaks, Calif.)2023
Endometriosis: Cellular and Molecular Mechanisms Leading to Fibrosis.
Review in Reproductive sciences (Thousand Oaks, Calif.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06792318 (Use of Fibroblast Activation Protein Inhibitor), which is not on this map. Cited by 72 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.
Use of Fibroblast Activation Protein Inhibitor (FAPI) PET-CT Before Surgery in Patient with Endometriosis
Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.
- The role of fibrosis in endometriosis: a systematic review.Human reproduction update · 2024Pooled it
- Endometriosis and Adenomyosis: Mechanotransduction, Microenvironment, and Mechanisms Beyond Lesions.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- FAP expression in deep and superficial endometriosis: Association with MRI and transvaginal ultrasound visibility.European journal of nuclear medicine and molecular imaging · 2026Article
- Phytochemicals Modulating Receptor Tyrosine Kinase Signaling Networks in Endometriosis.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Exosomal miR-21-5p from ectopic endometrial stromal cells drives fibrosis progression in endometriosis through direct VHL targeting.Human cell · 2026Article
- Targeting the IL-17C-M2 macrophage axis ameliorates fibrosis in endometriosis through MAPK/ERK signaling.Journal of translational medicine · 2026Article
- Collagen-binding ⁶⁸Ga-CBP8 PET/MR in Deep Pelvic Endometriosis: First-in-human Application.Molecular imaging and biology · 2026Article
- Targeting the Immune Network in Endometriosis: A Comprehensive Review of Pathogenesis, Immunomodulation, and Emerging Therapies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- The endometriosis-adenomyosis spectrum: shared pathophysiology and microenvironment-driven disease divergence.Reproductive biology and endocrinology : RB&E · 2026Review
- The lactate-myeloid-derived suppressor cells axis in endometriosis from molecular reprogramming to translational therapies: A review article.International journal of reproductive biomedicine · 2026Review
- Modulating IL-11-dependent matrix stiffness to delay ovarian aging.Nature aging · 2026Article
- Building Disease Models for Endometriosis: iPSCs as Game-Changers.International journal of molecular sciences · 2026Review
- Emerging signal transduction pathways and the role of bacterial extracellular vesicles linked to the pathogenesis of endometriosis.Communications medicine · 2026Review
- The Microbiota-Endometriosis Axis: An Immune-Endocrine Integration Model and Emerging Therapeutic Targets.International journal of molecular sciences · 2026Review
- Molecular Characterization of Ovarian Endometriosis in Saudi Arabian Women: Insights into Inflammatory, Autophagic, and Epigenetic Dysregulation.International journal of molecular sciences · 2026Article
- Uterine Vulnerability to Environmental PMInternational journal of molecular sciences · 2026Article
- Reduced type 2 epithelial-mesenchymal transition serves as a risk factor for the progression from endometriosis to endometriosis-associated ovarian cancer.Scientific reports · 2026Article
- Lactoferrin as a Non-Hormonal Therapeutic Candidate for Endometriosis: Mechanisms and Future Directions.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Physical Activity, Metabolic Dysfunction, and the Kynurenine Pathway in Endometriosis and Polycystic Ovary Syndrome: A Literature Review.Biomolecules · 2026Review
- Establishment of a xenograft model of endometriosis-associated fibrosis using human immortalized endometrial stromal cells overexpressing HOXC8.Scientific reports · 2026Article
12 more citing papers are in PubMed but not listed here.
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometriosis is a chronic inflammatory condition affecting women of reproductive age. A relevant feature of endometriosis is the presence of fibrotic tissue inside and around the lesions, thus contributing to the classic endometriosis-related symptoms, pain, and infertility. The molecular mechanisms responsible for the development of fibrosis in endometriosis are not yet defined. The present review aimed to examine the biological mechanisms and signalling pathways involved in fibrogenesis of endometriotic lesions, highlighting the difference between deep infiltrating and ovarian endometriosis. The main cell types involved in the development of fibrosis are platelets, myofibroblasts, macrophages, and sensory nerve fibers. Members of the transforming growth factor (TGF) -β family, as well as the receptor Notch, or the bioactive sphingolipid sphingosine 1-phosphate (S1P), play a role in the development of tissue fibrosis, resulting in their metabolism and/or their signalling pathways altered in endometriotic lesions. It is relevant the knowledge of the molecular mechanisms that guide and support fibrosis in endometriosis, to identify new drug targets and provide new therapeutic approaches to patients.
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.