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The role of microRNAs in endometriosis and associated reproductive conditions
Abstract
BACKGROUND: microRNAs (miRNAs) are short, single-stranded RNAs that regulate gene expression at the post-transcriptional level. Recent research has shown that miRNAs and their target mRNAs are differentially expressed in endometriosis and other disorders of the female reproductive system. Since miRNAs control a broad spectrum of normal and pathological cellular functions, they may play pivotal roles in the pathogenesis of these disorders. METHODS: A systematic review was undertaken of the published literature on; (i) the expression and functions of miRNAs in mammalian female reproductive tissues with a focus on endometriosis and the malignancies and fertility disorders related to this disease; and (ii) the potential roles played by validated mRNA targets of endometriosis-associated miRNAs. The current understanding of the biology of miRNAs is overviewed and the potential diagnostic and therapeutic potential of miRNAs in endometriosis is highlighted. RESULTS: The differential expression of miRNAs in endometriosis, and the putative molecular pathways constituted by their targets, suggests that miRNAs may play an important role in endometriotic lesion development. Models for miRNA regulatory functions in endometriosis are presented, including those associated with hypoxia, inflammation, tissue repair, TGFbeta-regulated pathways, cell growth, cell proliferation, apoptosis, extracellular matrix remodelling and angiogenesis. In addition, specific miRNAs which may be associated with malignant progression and subfertility in endometriosis are discussed. CONCLUSIONS: miRNAs appear to be potent regulators of gene expression in endometriosis and its associated reproductive disorders, raising the prospect of using miRNAs as biomarkers and therapeutic tools in endometriosis.
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“The authors conclude that miRNAs may play an important role in endometriotic lesion development, including regulatory functions associated with hypoxia, inflammation, tissue repair, TGF-b-regulated pathways, cell growth, cell proliferation, apoptosis, extracellular matrix remodeling, and angiogenesis.”
From Defining Future Directions for Endometriosis Research: Workshop Report From the 2011 World Congress of Endometriosis in Montpellier, France (2013) · cites this paper as [112]
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Metadata
- Authors
- Ohlsson Teague, E. M. C., Print, C. G., & Hull, M. L.
- Affiliations
- University of Auckland (NZ)
- The University of Adelaide (AU)
- Venue
- Human Reproduction Update
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-09-22
- Volume
- 16
- Issue
- 2
- Pages
- 142-165
- ISSN
- 1355-4786 (ISSN-L)
- 1460-2369
- OpenAlex
- W2142510444
- Cited by
- 309
- References
- 277
- Citations by year
- 2026: 9 · 2025: 17 · 2024: 12 · 2023: 13 · 2022: 21 · 2021: 14 · 2020: 25 · 2019: 24 · 2018: 27 · 2017: 25 · 2016: 21 · 2015: 25 · 2014: 19 · 2013: 23 · 2012: 13
- FWCI
- 1.60
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Human Reproduction Update (publishedVersion)
- PubMed (publishedVersion)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Endometriosis Research and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Extracellular vesicles in disease
- Keywords
- microRNA, endometriosis, female reproductive disorders, post-transcriptional regulation, endometriosis-associated malignancy, subfertility, hypoxia, inflammation, TGF-beta signaling, angiogenesis, extracellular matrix remodeling, apoptosis, cell proliferation, biomarkers, miRNA-based therapy
- MeSH terms
- Animals, Cell Transformation, Neoplastic, Endometriosis, Female, Genetic Markers, Genital Neoplasms, Female, Humans, Infertility, Female, Models, Genetic, Oocytes, Embryo Implantation, Pregnancy, Risk Factors, RNA, Neoplasm, MicroRNAs, Embryonic Development
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