The Pathological Role of miRNAs in Endometriosis

Mst Ismat Ara Begum, Chuan Lin, Lin Chuan, Seong‐Tshool Hong, Hee-Suk Chae, Heesuk Chae
Biomedicines · 2023 · vol. 11(11) , pp. 3087 · doi:10.3390/biomedicines11113087 · PMID:38002087 · W4388759732
review OA: gold CC0 ⤵ 11 in-corpus citations
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This review examines how altered microRNA expression in endometriotic lesions and eutopic endometrium contributes to endometriosis pathology and infertility, potentially leading to new diagnostics and therapeutics.

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Abstract

Association studies investigating miRNA in relation to diseases have consistently shown significant alterations in miRNA expression, particularly within inflammatory pathways, where they regulate inflammatory cytokines, transcription factors (such as NF-κB, STAT3, HIF1α), and inflammatory proteins (including COX-2 and iNOS). Given that endometriosis (EMS) is characterized as an inflammatory disease, albeit one influenced by estrogen levels, it is natural to speculate about the connection between EMS and miRNA. Recent research has indeed confirmed alterations in the expression levels of numerous microRNAs (miRNAs) in both endometriotic lesions and the eutopic endometrium of women with EMS, when compared to healthy controls. The undeniable association of miRNAs with EMS hints at the emergence of a new era in the study of miRNA in the context of EMS. This article reviews the advancements made in understanding the pathological role of miRNA in EMS and its association with EMS-associated infertility. These findings contribute to the ongoing pursuit of developing miRNA-based therapeutics and diagnostic markers for EMS.

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endometriosisinfertility

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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.

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