Apparent lncRNAs involvement in pathogenesis of endometriosis

Katarzyna Kwas, Maria Szubert, Jacek R. Wilczyński
In: Journal of Endometriosis and Pelvic Pain Disorders · 2024 · vol. 17(1) , pp. 39–48 · doi:10.1177/22840265241298743 · W4404665395
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⚙ AI-generated summary by claude@2026-06, 2026-06-09 ⓘ

This review summarizes lncRNAs found to influence endometriosis pathogenesis and their potential role in its transition to associated ovarian cancer.

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Abstract

Endometriosis is an estrogen-dependent, debilitating gynecologic disease impacting millions of women globally. One of the main characteristics of this benign condition is the presence of endometrial-like tissue outside the uterus, causing dysmenorrhea, chronic pelvic pain, and infertility. However, despite many reports on the origin and molecular pathogenesis of endometriosis, the etiology of this disease has not been fully explored yet. Recently, significant attention has been paid to long noncoding RNAs (lncRNAs). Numerous studies focused on exploring the association between lncRNAs and the progression of various human diseases. LncRNAs function as competing endogenous RNAs (ceRNAs) interacting with microRNAs as a “sponge” to regulate cell functions. According to multiple studies, lncRNAs seem to have the potential as markers for diagnosing, and monitoring progression and staging in endometriosis. In this review, we summarized the lncRNAs that were found to influence the pathogenesis of endometriosis. Furthermore, we tried to assess its potential in the process of endometriosis transition from benign through atypical forms, up to EAOC (Endometriosis Associated Ovarian Cancer).

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Condition tags

endometriosischronic_pelvic_paindysmenorrheainfertility

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 (58)

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