Exploring the role of epigenetics in the processes related to the development of endometrosis in the mare
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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.
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A better understanding of the epigenetic mechanisms involved in the development and
progression of endometrial fibrosis could help to reveal the mechanisms behind the
fibrotic process. Epigenetic alterations, such as aberrant DNA methylation, ncRNA
dysregulation, or histone modification, drive persistent fibroblast activation and
excessive ECM accumulation, driving the development of endometrial fibrosis.
Importantly, the reversible nature of epigenetic changes offers promising opportunities
for targeted therapies, including DNMT inhibitors, miRNA modulators, and histone
deacetylase (HDAC) inhibitors that are currently under investigation. Despite extensive
research, there is an absence of effective treatments for mare endometrial fibrosis.
This emphasises the urgent need for novel strategies that could be derived from
epigenetic mechanisms. Understanding epigenetic contributions can not only advance
scientific knowledge but also potentially improve reproductive efficiency in mare with
endometrosis, offering significant economic benefits for the breeding industry.
Additionally, current results highlighting epigenetics involvement in endometrosis
pathogenesis make them promising candidates for the identification of markers of
endometrosis progression [ 94 , 130 , 148 ].
Specific epigenetic changes could serve early indicators of disease and therapeutic
targets. For example, epigenetic research could enable the development of diagnostic
tests using altered DNA methylation patterns or lncRNAs for the detection of early
conditions. The growing recognition of the importance of the epigenetic signature, as
both diagnostic markers and therapeutic targets, may open new possibilities for the
management and treatment of equine endometrosis. Moreover, a better understanding of the
epigenetic mechanisms is expected to lead to more accurate diagnoses and improved
therapeutic strategies to restore fertility and uterine tissue function in mares. This
integrative approach aims to translate molecular insights into effective clinical
treatments for equine endometrosis.
Coi Statement
The authors have nothing to declare.
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- europepmc
- last seen: 2026-08-16T09:21:09.727480+00:00
- pubmed
- last seen: 2026-08-19T06:03:54.274980+00:00
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Courtesy of the U.S. National Library of Medicine
Courtesy of the U.S. National Library of Medicine