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Biomedicines · 2025

Long noncoding RNAs and microRNAs in Endometriosis.

СтатьяОбзорНазвание и аннотация: Перевод в очереди
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Muhaxhiri Edi, Debeljak Maruša, Trebušak Podkrajšek Katarina, Ban Frangež Helena

Аннотация

Endometriosis represents a prevalent gynaecological disorder, impacting around 10% of the female population and affecting as many as 50% of women who are facing challenges with infertility. The pathogenesis of the disease encompasses intricate processes such as the formation of adhesions, degradation of the extracellular matrix, angiogenesis, increased cell proliferation, impaired apoptosis, and dysregulation of the immune response. Although endometriosis is common, its precise etiology remains unidentified, despite various hypotheses being suggested. Recent findings underscore the significance of non-coding RNAs, specifically long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), which have been identified as important regulators in the development of endometriosis. This literature review integrates findings from various transcriptomic and molecular studies to distinguish between lncRNAs and miRNAs that are associated with direct pathogenic roles and those that simply represent altered gene expression profiles in endometriosis. Particular long non-coding RNAs, such as H19, MALAT1, and LINC01116, are associated with chromatin remodeling, functioning as competitive endogenous RNAs, and influencing critical signaling pathways. Concurrently, specific microRNAs, including the miR-200 family, miR-145, and let-7b, seem to govern processes like epithelial-to-mesenchymal transition, angiogenesis, and cell adhesion. The findings highlight the significant potential of non-coding RNAs to serve as biomarkers for diagnostic purposes and as innovative therapeutic targets. Subsequent research endeavours ought to focus on corroborating these findings and elucidating the specific pathogenic roles of these non-coding RNAs in the context of endometriosis.

ИП Урсолов Владлен Сергеевич

ИНН 500118482352 · ОГРНИП 314500117700049

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