Cañete, AnaCano, ElenaMuñoz-Chápuli, RamónCarmona, Rita2023-01-252023-01-252017-02-20http://hdl.handle.net/10668/10897Vitamin A is an essential micronutrient throughout life. Its physiologically active metabolite retinoic acid (RA), acting through nuclear retinoic acid receptors (RARs), is a potent regulator of patterning during embryonic development, as well as being necessary for adult tissue homeostasis. Vitamin A deficiency during pregnancy increases risk of maternal night blindness and anemia and may be a cause of congenital malformations. Childhood Vitamin A deficiency can cause xerophthalmia, lower resistance to infection and increased risk of mortality. RA signaling appears to be essential for expression of genes involved in developmental hematopoiesis, regulating the endothelial/blood cells balance in the yolk sac, promoting the hemogenic program in the aorta-gonad-mesonephros area and stimulating eryrthropoiesis in fetal liver by activating the expression of erythropoietin. In adults, RA signaling regulates differentiation of granulocytes and enhances erythropoiesis. Vitamin A may facilitate iron absorption and metabolism to prevent anemia and plays a key role in mucosal immune responses, modulating the function of regulatory T cells. Furthermore, defective RA/RARα signaling is involved in the pathogenesis of acute promyelocytic leukemia due to a failure in differentiation of promyelocytes. This review focuses on the different roles played by vitamin A/RA signaling in physiological and pathological mouse hematopoiesis duddurring both, embryonic and adult life, and the consequences of vitamin A deficiency for the blood system.enAttribution 4.0 Internationalhttp://creativecommons.org/licenses/by/4.0/embryoshematopoiesisleukemiaretinoic acidvitamin Avitamin A deficiencyAnemia, Iron-DeficiencyAnimalsCell DifferentiationDisease Models, AnimalEmbryonic DevelopmentEpigenesis, GeneticErythropoiesisErythropoietinFemaleGranulocytesHematopoiesisHumansLeukemia, Promyelocytic, AcutePregnancyReceptors, Retinoic AcidSignal TransductionTretinoinVitamin AVitamin A Deficiencyresearch article28230720open access10.3390/nu90201592072-6643PMC5331590https://www.mdpi.com/2072-6643/9/2/159/pdf?version=1487578571https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5331590/pdf