Pathogenesis of endometriosis: the role of genetics, inflammation and oxidative stress

review OA: closed CC0 ⤵ 100 in-corpus citations
Limited metadata. Only one source feed has indexed this record so far — no abstract, full text, or open-access copy is available through Endo Lab. The publisher's page (linked below) is the canonical location for the actual content. If you have institutional access, use "Find at my library".
AI-generated summary by claude@2026-06+body, 2026-06-08

This literature review examines genetic abnormalities, inflammation, and oxidative stress as contributing factors to the pathogenesis of endometriosis.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

AI-generated deep summary by claude@2026-06, 2026-06-08

This paper is a literature review on the unresolved multifactorial etiology of endometriosis, focusing on how genetic abnormalities, inflammatory activity, and oxidative stress may contribute to disease pathogenesis. It synthesizes evidence from studies examining susceptibility-related genetic variants (including those in detoxification and hormone-related pathways) and from research characterizing chronic inflammatory and oxidative alterations. A key finding is that the reviewed body of work links predisposition to endometriosis with interactions among genetics, inflammation, and oxidative stress, including iron- and NF-κB–related considerations. The main limitation is that, as a review, it does not present new experimental data and the multifactorial mechanisms remain incompletely resolved. This paper is centrally about endometriosis — it reviews genetic, inflammatory, and oxidative-stress roles in endometriosis pathogenesis, with some genetic references also mentioning adenomyosis.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Endometriosis Genetic Predisposition to Disease Inflammation Oxidative Stress Endometriosis Female Humans Inflammation

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 (81)

Cited by (50)

Source provenance

europepmc
last seen: 2026-06-13T06:22:48.782012+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:16:17.081435+00:00
License: CC0 · commercial use OK