Pathogenesis of endometriosis: Interaction between Endocrine and inflammatory pathways

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This paper explores how endocrine and inflammatory pathways interact to contribute to the development of endometriosis.

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Abstract

Despite an estimated prevalence of 11% in women and plausible historical descriptions dating back to the 17th century, the etiology of endometriosis remains poorly understood. Classical theories of the histological origins of endometriosis are reviewed below. Clinical presentations are variable, and signs and symptoms do not correlate well with the extent of disease. In this summary, we have attempted to synthesize the growing evidence that hormonal and immune factors conspire to activate a local inflammatory microenvironment that encourages endometriosis to persist and elaborate mediators of its two cardinal symptoms: pain and infertility. Surprisingly, in the search for novel therapeutics for medical treatment of endometriosis, some compounds appear to have dual pharmacological functions, simultaneously modifying the endocrine and immune system facets of this complex gynecologic syndrome. We predict that these lead drugs will provide more therapeutic choices for patients in the future.

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Condition tags

endometriosischronic_pelvic_pain

MeSH descriptors

Endocrine System Endometriosis Immune System Endocrine System Endocrine System Endometriosis Endometriosis Endometriosis Female Humans Immune System Immune System Infertility, Female Infertility, Female Inflammation Inflammation Inflammation Pelvic Pain Pelvic Pain

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (100)

Cited by (50)

Source provenance

europepmc
last seen: 2026-08-26T06:08:41.316361+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
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License: CC0 · commercial use OK