Promising therapeutic targets of endometriosis obtained from microRNA studies
Nine overexpressed microRNAs were identified as inducing endometriosis characteristics, with their downstream target molecules proposed as promising therapeutic targets.
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This paper reviews prior studies on aberrantly expressed microRNAs (miRNAs) in endometriosis, identifying nine miRNAs reported as overexpressed and examining their effects in endometriotic tissues and cells. The authors report that these overexpressed miRNAs promote endometriosis-associated phenotypes, including inhibition of apoptosis and decidualization, and increased fibrogenesis, invasion, migration, proliferation, attachment to extracellular matrix, inflammation, and angiogenesis. Based on the downstream target molecules of these miRNAs (e.g., early growth response protein-1, ERK, matrix metallopeptidase 1, STAT3, COX-2, PI3K/AKT, mTOR, and VEGF-A), the paper proposes these molecules as promising therapeutic targets. It does not present new experimental data and instead synthesizes literature, with the limitation that complex miRNA mechanisms and clinical treatment relationships are inferred rather than tested within this review. This paper is centrally about endometriosis — it synthesizes endometriosis-associated overexpressed miRNAs and their downstream targets as candidate therapeutic targets.
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Cited by (6)
- Evaluating the effect of exosome-encapsulated miR-4289 on menstrual blood-derived mesenchymal stem cells from endometriosis patients 2025
- Overexpression of hsa-miR-132-5p in ovarian endometriotic stromal cells promoted acquisition of endometriotic phenotype 2025
- Evaluating the Effect of Exosome-Encapsulated miR-4289 on Menstrual Blood-Derived Mesenchymal Stem Cells from Endometriosis Patients 2025
- Circ_0001495 influences the development of endometriosis through the miRNA-34c-5p/E2F3 axis 2024
- Advances in Treatment of Endometriosis 2022
- Promising therapeutic targets of endometriosis obtained from microRNA studies 2021
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- europepmc
- last seen: 2026-06-14T06:08:20.186862+00:00
- openalex
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- pubmed
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