Physiological and pathological implications of retinoid action in the endometrium

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.

Fertility performance and the predictive value of the endometriosis fertility index staging system in women with recurrent endometriosis

“…First, the eutopic endometrium is resistant to the selective actions of progesterone that affect downstream P target genes and ultimately leads to decidualization [13] ; Second, the detrimental effects of the inflammatory process related to endometriosis can impede the progression of early embryos during the first trimester of pregnancy [14] ; Third, alterations in humoral and cell-mediated immunity in the endometrium have been discussed in the context of pregnancy failure in women with endometriosis. [15,16] However, these possibilities are difficult to demonstrate and remained speculative. More evidence is needed.…”

Retinoid Signaling Controlled by SRC-2 in Decidualization Revealed by Transcriptomics

“…2007). Retinoid signaling is known to control cell differentiation, proliferation, and cell survival in numerous physiological and pathological contexts (Jiang et al . 2018).…”

Progesterone induces cell apoptosis via the CACNA2D3/Ca2+/p38 MAPK pathway in endometrial cancer

“…Therefore, elucidation of the molecular mechanisms underlying EC may assist in identifying and developing promising therapeutic targets and prognostic markers. The ovarian steroid hormones, estrogen and progesterone are essential regulators of uterine biology (5). The endometrium is particularly sensitive to steroid hormones, and long-term exposure to estrogens, unopposed by progesterone, may be a predisposing factor to EC (6).…”