Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (535 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A condition in which functional endometrial tissue is present outside the uterus. It is often confined to the pelvis involving the ovary, the ligaments, cul-de-sac, and the uterovesical peritoneum.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Endometrioses; Endometrioma; Endometriomas.
Where it fits in the MeSH classification
- Broader topics
- Genital Diseases, Female
Related concepts
Research landscape
PubMed indexes 29,583 records tagged with the MeSH heading “Endometriosis” (counts retrieved 2026-11-04). 7,826 of them (26.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 8,648 records.
Reviews account for 5,124 records (17.3%) and meta-analyses for 487. Randomized controlled trials number 668 (2.3%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 8,648 |
| 2000-2009 | 5,329 |
| 2010-2019 | 7,780 |
| 2020 onward | 7,826 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 5,124 | 17.3% |
| Meta-analyses | 487 | 1.6% |
| Randomized controlled trials | 668 | 2.3% |
Method: PubMed query "Endometriosis"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in kidney, urology and women's health
Kidney, urinary and reproductive health research uses lab markers (such as creatinine), imaging, symptom scores and registry data on pregnancy and birth. Findings about pregnancy are especially sensitive to who was studied and when in pregnancy exposure occurred. Nothing on this page is advice about treatment, fertility or pregnancy; speak to a qualified clinician. Check the population, the outcome measured and whether the study accounted for other health differences between groups.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Immune dysregulation in endometriosis: the T cell perspective | 2026 | Review article Design not recorded in structured metadata | 6 | cc by PMID 42023240 · DOI · PMC13096776 |
| Clinical and endocrine effects of pharmacological therapy in endometriosis: a systematic review and meta-analysis | 2026 | Meta-analysis Design not recorded in structured metadata | 3 | cc by PMID 41993993 · DOI · PMC13078990 |
| Human Endometriotic Lesion-Derived Small Extracellular Vesicles Impair Macrophage Function in the Peritoneal Microenvironment | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41711665 · DOI · PMC12919373 |
Immune dysregulation in endometriosis: the T cell perspective [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Endometriosis is a chronic inflammatory, hormone dependent disorder that affects more than 200 million women worldwide.
- Closing excerpt
- A systems-level understanding of T cell roles within the endocrine-immune microenvironment is essential for developing targeted immunotherapies and personalized interventions for this globally prevalent disease.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (193 words)
Endometriosis is a chronic inflammatory, hormone dependent disorder that affects more than 200 million women worldwide. Immune dysfunction has emerged as one of the predominant mechanisms facilitating endometriosis lesion growth and survival. In particular, T cell subsets are predominant effector immune cells within the complex endometriosis lesion microenvironment. T cell biology encompasses a highly regulated and diverse network of cellular differentiation, antigen recognition, and immune regulation, all of which play critical roles in immune homeostasis. This complexity becomes particularly relevant in endometriosis, as autologous lesions evade immune clearance within this sterile, non-pathogen-driven inflammatory milieu, highlighting a failure of immune surveillance and debris clearance. Indeed, aberrant T cell phenotypes, including skewed Th2 and regulatory subsets, promote an anti-inflammatory and tissue-remodeling environment in endometriosis. Despite advances in characterizing immune cell subsets, the mechanisms underlying T cell dysfunction and lesion persistence remain poorly defined. Here, we provide comprehensive insights into the diverse T cell subsets infiltrating endometriosis lesions and associated mechanisms that potentially contribute to endometriosis lesion establishment and subsequent survival. A systems-level understanding of T cell roles within the endocrine-immune microenvironment is essential for developing targeted immunotherapies and personalized interventions for this globally prevalent disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42023240 · DOI · PMC13096776
Clinical and endocrine effects of pharmacological therapy in endometriosis: a systematic review and meta-analysis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundEndometriosis, PCOS, adenomyosis, and dysmenorrhea are major illnesses.
- Closing excerpt
- Different endocrine therapies based on the patient's specific characteristics and the degree of tolerability should be used to achieve the maximum effect of clinical outcomes.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (141 words)
BackgroundEndometriosis, PCOS, adenomyosis, and dysmenorrhea are major illnesses. Hormonal as well as non-hormonal treatments were evaluated for COCs, progestins, GnRH analogues, LNG-IUS, relugolix, and adjunctive therapies. These treatments resulted in the categorization of the benefits in varying degrees.Methods149 clinical trials have been included. Evaluating the methodological quality was done through the Jadad scale, while the GRADE criteria were used to assess the reliability of the evidence. When these data were available, effect sizes, standardized mean differences (SMD), 95% confidence intervals (CI), and p-values were extracted.ResultsIt was observed that COCs and progestins considerably lowered pelvic pain and menstrual irregularities (SMD -0.35 to -0.58, 95% CI -0.90 to -0.08, pConclusionsEndometriosis disorder have been treated well with hormonal therapies. Different endocrine therapies based on the patient's specific characteristics and the degree of tolerability should be used to achieve the maximum effect of clinical outcomes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41993993 · DOI · PMC13078990
Human Endometriotic Lesion-Derived Small Extracellular Vesicles Impair Macrophage Function in the Peritoneal Microenvironment [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Endometriosis (EM) is a chronic inflammatory disease that affects ∼10% of women during reproductive age.
- Closing excerpt
- This study provides the first thorough characterisation of EE-derived sEVs utilising EEO models in EM and demonstrates their potential immunomodulatory role in the peritoneal microenvironment via CD47/SIRP-α signalling.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (201 words)
Endometriosis (EM) is a chronic inflammatory disease that affects ∼10% of women during reproductive age. It is characterised by ectopic (ECT) growth of endometrial-like tissue mainly in the pelvic cavity. Small extracellular vesicles (sEVs) mediate cellular interactions, but their function remains poorly understood in the pathogenesis of EM. 3D endometrial epithelial organoids (EEOs) from ECT lesions and eutopic (EUT) endometrium from EM patients and controls were established to investigate sEVs. Multiplex bead-based flow cytometry revealed CD133/1 and EpCAM as dominant markers on EEO-sEVs, with ECT EEO-sEVs showing upregulation of CD44, CD29 and downregulation of EpCAM compared to EUT EEO-sEVs. Peritoneal fluid (PF)-sEVs displayed high and correlated CD133/1 and EpCAM expression, indicating a major contribution from endometrial epithelial (EE) cells, alongside sEVs of lymphocyte and endothelial origin. Functionally, both ECT EEO-sEVs and PF-sEVs from EM patients significantly suppressed macrophage phagocytosis, as assessed by pH-sensitive fluorescent bioparticles. The effect was reversed by CD47 blockade. The coexpression of CD47 with CD133/1 and EpCAM on PF-sEVs indicates the involvement of EE cell-derived sEVs in CD47/SIRP-α mediated suppression. This study provides the first thorough characterisation of EE-derived sEVs utilising EEO models in EM and demonstrates their potential immunomodulatory role in the peritoneal microenvironment via CD47/SIRP-α signalling.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41711665 · DOI · PMC12919373
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The impact of excision of ovarian endometrioma on ovarian reserve: a systematic review and meta-analysis [4]
- Research article Reproductive, obstetric, and perinatal outcomes of women with adenomyosis and endometriosis: a systematic review and meta-analysis [5]
- Research article The genetic basis of endometriosis and comorbidity with other pain and inflammatory conditions [6]
- Research article The association between endometriosis and autoimmune diseases: a systematic review and meta-analysis [7]
- Research article Imaging modalities for the non-invasive diagnosis of endometriosis [8]
- Research article The impact of endometrioma on IVF/ICSI outcomes: a systematic review and meta-analysis [9]
Full-text reviews on EvidenceLib
Open-access review articles about this topic, reproduced in full with authors, licence and references.
The role of CD8+ T cells in endometriosis: a systematic review
Ana Kisovar, Christian M. Becker, Ingrid Granne et al. · Frontiers in Immunology 2023 · CC BY 4.0
Endometriosis and Risk of Adverse Pregnancy Outcome: A Systematic Review and Meta-Analysis
Kjerstine Breintoft, Regitze Pinnerup, Tine Brink Henriksen et al. · Journal of Clinical Medicine 2021 · CC BY 4.0
The Pathogenesis of Endometriosis: Molecular and Cell Biology Insights
Antonio Simone Laganà, Simone Garzon, Martin Götte et al. · International Journal of Molecular Sciences 2019 · CC BY 4.0
References
- Sisnett DJ, Zutautas KB, Vo DHN, Ravishanker K, Holmes JP, Wodz A, et al.. Immune dysregulation in endometriosis: the T cell perspective. . 2026. PMID 42023240 · DOI · PMC13096776
- Sun R, Xu H, Ma R, Xu J, Liu Y, Mao D. Clinical and endocrine effects of pharmacological therapy in endometriosis: a systematic review and meta-analysis. . 2026. PMID 41993993 · DOI · PMC13078990
- Wang Y, Jin Z, Blatchford AF, Hosh B, Amer M, Akhatova A, et al.. Human Endometriotic Lesion-Derived Small Extracellular Vesicles Impair Macrophage Function in the Peritoneal Microenvironment. . 2026. PMID 41711665 · DOI · PMC12919373
- Raffi F, Metwally M, Amer S. The impact of excision of ovarian endometrioma on ovarian reserve: a systematic review and meta-analysis. J Clin Endocrinol Metab. 2012. PMID 22723324 · DOI
- Horton J, Sterrenburg M, Lane S, Maheshwari A, Li TC, Cheong Y. Reproductive, obstetric, and perinatal outcomes of women with adenomyosis and endometriosis: a systematic review and meta-analysis. Hum Reprod Update. 2019. PMID 31318420 · DOI
- Rahmioglu N, Mortlock S, Ghiasi M, Møller PL, Stefansdottir L, Galarneau G, et al.. The genetic basis of endometriosis and comorbidity with other pain and inflammatory conditions. Nat Genet. 2023. PMID 36914876 · DOI · PMC10042257
- Shigesi N, Kvaskoff M, Kirtley S, Feng Q, Fang H, Knight JC, et al.. The association between endometriosis and autoimmune diseases: a systematic review and meta-analysis. Hum Reprod Update. 2019. PMID 31260048 · DOI · PMC6601386
- Nisenblat V, Bossuyt PM, Farquhar C, Johnson N, Hull ML. Imaging modalities for the non-invasive diagnosis of endometriosis. Cochrane Database Syst Rev. 2016. PMID 26919512 · DOI · PMC7100540
- Hamdan M, Dunselman G, Li TC, Cheong Y. The impact of endometrioma on IVF/ICSI outcomes: a systematic review and meta-analysis. Hum Reprod Update. 2015. PMID 26168799 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.