Physiological and pathological implications of retinoid action in the endometrium

J Endocrinol. 2018 Mar;236(3):R169-R188. doi: 10.1530/JOE-17-0544. Epub 2018 Jan 3.

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.

Keywords: endometrial stroma; endometriosis; implantation; retinoids.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Aldehyde Dehydrogenase / genetics
  • Aldehyde Dehydrogenase 1 Family
  • Animals
  • Decidua / physiopathology
  • Embryo Implantation / physiology
  • Endometriosis / etiology
  • Endometriosis / physiopathology
  • Endometrium* / blood supply
  • Endometrium* / physiopathology
  • Female
  • Gene Expression
  • Gene Expression Regulation / physiology
  • Humans
  • Mice
  • Neovascularization, Physiologic / physiology
  • Receptors, Retinoic Acid / genetics
  • Retinal Dehydrogenase / genetics
  • Retinoids / adverse effects*
  • Retinoids / metabolism*
  • Retinoids / physiology
  • Signal Transduction
  • Stromal Cells

Substances

  • Receptors, Retinoic Acid
  • Retinoids
  • Aldehyde Dehydrogenase 1 Family
  • Aldehyde Dehydrogenase
  • ALDH1A1 protein, human
  • ALDH1A2 protein, human
  • Retinal Dehydrogenase