Abstract
Background: Endometriosis (EMS) is a gynecological disease defined by the translocation
and growth of endometrial tissue in other tissues or organs outside the uterus. Its clinical manifestations
are dysmenorrhea, irregular menstruation, and even infertility. Although EMS is a benign
disease, it has the characteristics of malignant tumor and the potential of malignant transformation.
Recent studies have found that EMS may involve epigenetic changes and that various epigenetic aberrations,
especially aberrant DNA methylation may play an essential role in the pathogenesis of EMS.
Previous studies have elucidated the epigenetic regulators of EMS and reported variations in epigenetic
patterns
of genes known to be associated with abnormal hormonal, immune, and inflammatory
states of EMS. With the development of high-throughput sequencing and other biomolecular technologies,
we have a better understanding of genome-wide methylation in EMS.
Objective: This article will discuss the potentiality of targeting DNA methylation as the therapeutic
approach for EMS.
Results: This article reviews the role of DNA methylation in the pathophysiology of EMS and provides
insight into a novel therapeutic approach for EMS by targeting DNA methylation modifiers. We
also review the current progress in using DNA methylation inhibitors in EMS therapy and the potential
promise and challenges ahead.
Conclusion: Aberrant DNA methylation plays an essential role in the pathogenesis of EMS and epigenetic
agents targeting DNA methyltransferases are expected to be the theoretical basis for the new
treatment of EMS.
Keywords:
Endometriosis, aberrant DNA methylation, gene, pathway, DNMTs, DNMTs inhibitors.
Graphical Abstract
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