Exploring the role of epigenetics in the processes related to the development of endometrosis in the mare
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CC-BY-NC-ND-4.0
Abstract
Endometrosis is a chronic degenerative condition of the mare endometrium characterized by progressive fibrosis and glandular alterations that impair uterine function and fertility. Its pathogenesis involves persistent inflammation, the activation of myofibroblasts, and the accumulation of extracellular matrix (ECM), leading to disrupted glandular secretion and compromised maintenance of pregnancy. While histopathological studies of endometrosis are well described, the underlying molecular mechanisms remain incompletely understood. Emerging evidence highlights the crucial role of epigenetic regulation, particularly DNA methylation, non-coding RNAs (ncRNA), and histone modifications in modulating the gene networks that drive fibrosis. Altered DNA methylation patterns in key profibrotic and antifibrotic genes modulate collagen deposition and ECM turnover, while specific ncRNAs regulate genes involved in fibrotic and inflammatory pathways. Recent studies suggest that endometrosis progression in mares is accompanied by dynamic changes in the epigenetic landscape of both the endometrium and myometrium, highlighting the role of epigenetic regulation in this condition. This review synthesizes current knowledge on the epigenetic mechanisms implicated in mare endometrosis, focusing on DNA methylation-mediated regulation of fibrosis-related genes, histone modification, and changes in ncRNA expression in endometrium and/or myometrium during the progression of fibrotic changes, and their impact on the pathogenesis of this condition. Understanding these molecular processes is essential for identifying novel diagnostic biomarkers and developing targeted therapies to improve reproductive outcomes in affected mares.
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Review
Exploring the role of epigenetics in the processes related to the development of endometrosis in the mare
2026 Volume 72 Issue 3 Pages 274-281
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Abstract
Endometrosis is a chronic degenerative condition of the mare endometrium characterized by progressive fibrosis and glandular alterations that impair uterine function and fertility. Its pathogenesis involves persistent inflammation, the activation of myofibroblasts, and the accumulation of extracellular matrix (ECM), leading to disrupted glandular secretion and compromised maintenance of pregnancy. While histopathological studies of endometrosis are well described, the underlying molecular mechanisms remain incompletely understood. Emerging evidence highlights the crucial role of epigenetic regulation, particularly DNA methylation, non-coding RNAs (ncRNA), and histone modifications in modulating the gene networks that drive fibrosis. Altered DNA methylation patterns in key profibrotic and antifibrotic genes modulate collagen deposition and ECM turnover, while specific ncRNAs regulate genes involved in fibrotic and inflammatory pathways. Recent studies suggest that endometrosis progression in mares is accompanied by dynamic changes in the epigenetic landscape of both the endometrium and myometrium, highlighting the role of epigenetic regulation in this condition. This review synthesizes current knowledge on the epigenetic mechanisms implicated in mare endometrosis, focusing on DNA methylation-mediated regulation of fibrosis-related genes, histone modification, and changes in ncRNA expression in endometrium and/or myometrium during the progression of fibrotic changes, and their impact on the pathogenesis of this condition. Understanding these molecular processes is essential for identifying novel diagnostic biomarkers and developing targeted therapies to improve reproductive outcomes in affected mares.
© 2026 The Society for Reproduction and Development
This article is licensed under a Creative Commons [Attribution-NonCommercial-NoDerivatives 4.0 International] license.
https://creativecommons.org/licenses/by-nc-nd/4.0/
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License: CC-BY-NC-ND-4.0