Epigenetics’ responsibility in endometriosis: A comprehensive assessment

Abstract

Endometriosis is a chronic inflammatory disease characterized by the presence of endometrial-like tissue outside the uterus, affecting women of reproductive age. Despite extensive research, its pathophysiology remains unclear, with genetic, hormonal, and environmental factors playing interconnected roles. Epigenetic processes, including non-coding RNAs, histone modifications, and DNA methylation, have been implicated in the genesis and progression of endometriosis. These modifications impact physiological functions such as inflammation, cell division, apoptosis, and hormone sensitivity. Recent findings on epigenetic alterations in endometriosis highlight their role in the abnormal behavior of ectopic endometrial-like cells. Aberrant DNA methylation patterns in genes related to immunological control and oestrogen metabolism contribute to the invasiveness and durability of lesions. Histone modifications, such as methylation and acetylation, regulate gene expression by altering chromatin structure. Non-coding RNAs, particularly microRNAs, influence tissue remodeling and inflammation. Given the reversible nature of epigenetic modifications, they present promising therapeutic targets for innovative treatment strategies. Epigenetic-based therapies aim to reverse pathological gene expression patterns, offering hope for more personalized and effective management of endometriosis. Further research is needed to fully utilize epigenetic processes in treating this debilitating disease.