Epigenetics of Uterine Physiology and Disease

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About this Research Topic

Submission deadlines

  1. Manuscript Submission Deadline 3 February 2026

  2. This Research Topic is currently accepting articles.

Background

The uterus is one of the most dynamic organs in the human body, undergoing multiple physiological changes throughout a woman's life, encompassing menstrual cycles, pregnancy, menopause, and post-menopause. Recently, the study of epigenetic mechanisms in uterine physiology has gained significant importance, as it has been demonstrated that DNA methylation, post-translational histone modifications, chromatin remodeling, and non-coding RNAs play fundamental roles in regulating the expression of genes crucial for the function of this organ. Furthermore, there is an excellent opportunity to deepen our understanding of this area and its implications for pathologies affecting a large proportion of reproductive-age women, which can substantially impact their quality of life.

The objective of this Research Topic is to explore and expand our knowledge of the epigenetic mechanisms involved in the physiology of the uterine tissues, primarily the endometrium and myometrium, as well as the phenotypic and functional changes of these tissues at different stages of a woman's life. Additionally, we aim to compile a collection of cutting-edge studies that determine the participation of these mechanisms in uterine-associated pathologies, such as endometriosis, adenomyosis, endometritis, Asherman syndrome, endometrial hyperplasia, endometrial cancer, leiomyoma, infertility, among others. By addressing these intriguing topics, this issue seeks to bridge the knowledge gap in clinical epigenetics applied to women's reproductive health.

This Research Topic welcomes contributions of any type of accepted articles in the Epigenomics and Epigenetics section (Original Research, Brief Research Report, Mini-Review, Systematic Review, and Perspectives). Submissions focusing on epigenetic mechanisms may be related to, but are not limited to, the following topics:

- Physiology of the uterus and its component tissues.

- Phenotypic changes occurring in uterine tissues during embryonic development, menstrual cycles, menopause, pregnancy, childbirth, and postpartum.

- Effects of drugs, hormone receptor agonists, contraceptives, etc., on uterine tissues.

- Endometrial alterations occurring in not-uterine reproductive diseases (e.g., polycystic ovary syndrome).

- Uterine pathologies such as endometriosis, adenomyosis, endometritis, Asherman syndrome, infertility, endometrial hyperplasia, endometrial cancer, and leiomyoma, among others.

- Diagnostic or prognostic biomarkers for diseases affecting the uterus.

Papers that do not adhere to Frontiers' ethical standards or those consisting solely of previously published data analysis without any experimental validation will not be considered.

Article types and fees

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

  • Brief Research Report
  • Data Report
  • Editorial
  • FAIR² Data
  • General Commentary
  • Hypothesis and Theory
  • Methods
  • Mini Review
  • Opinion

Articles that are accepted for publication by our external editors following rigorous peer review incur a publishing fee charged to Authors, institutions, or funders.

Keywords: uterus, endometrium, myometrium, pregnancy, labour, menstrual cycle, endometriosis, adenomyosis, endometritis, Asherman syndrome, endometrial hyperplasia, endometrial cancer, leiomyoma, infertility, aging, menopause, epigenetics, chromatin, DNA methylatio

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Topic editors

Manuscripts can be submitted to this Research Topic via the main journal or any other participating journal.

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