Accepted Preprint (first posted online 3 January 2018)

    Physiological and pathological implications of retinoid action in the endometrium

    1. Xu Zhou
    1. Y Jiang, College of Animal Sciences, Jilin University, Changchun, China
    2. L Chen, College of Animal Sciences, Jilin University, Changchun, United States
    3. R Taylor, Departments of Obstetrics and Gynecology and Molecular Medicine and Translational Sciences, Wake Forest University School of Medicine, Winston-Salem, United States
    4. C Li, College of Animal Sciences, Jilin University, Changchun, China
    5. X Zhou, College of Animal Sciences, Jilin University, Changchun, China
    1. Correspondence: Xu Zhou, Email: xzhou65{at}vip.sina.com

    Abstract

    Retinol (vitamin A) and its derivatives, collectively known as retinoids, are required for maintaining vision, immunity, barrier function, reproduction, embryogenesis, and cell proliferation and differentiation. Despite the fact that most events in the endometrium are predominantly regulated by steroid hormones (estrogens and progesterone), accumulating evidence shows that retinoid signaling is also involved in the development and maintenance of the endometrium, stromal decidualization, and blastocyst implantation. Moreover, aberrant retinoid metabolism seems to be a critical factor in the development of endometriosis, a common gynecological disease which affects up to 10% of reproductive-age women and is characterized by the ectopic localization of endometrial-like tissue in the pelvic cavity. This review summarizes recent advances in research on the mechanisms and molecular actions of retinoids in normal endometrial development and physiological function. The potential roles of abnormal retinoid signaling in endometriosis are also discussed. The objectives are to identify limitations in current knowledge regarding the molecular actions of retinoids in endometrial biology and to stimulate new investigations toward the development potential therapeutics to ameliorate or prevent endometriosis symptoms.

    • Received 19 October 2017
    • Received in final form 19 December 2017
    • Accepted 3 January 2018
    • Accepted Preprint first posted online on 3 January 2018

    This Article

    1. J Endocrinol JOE-17-0544
    1. Abstract

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