ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013
The retinaldehyde reductase DHRS3 is essential for preventing the formation of excess retinoic acid during embryonic development.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 125 citations in OpenAlex.
- Key molecular networks underlying retinol's biphasic effects on cell proliferation through multi-omics integrative analysis using genome-scale metabolic modeling.Synthetic and systems biotechnology · 2027Article
- Retinoic acid in health and disease.Signal transduction and targeted therapy · 2026Review
- The retinol-metabolizing enzyme DHRS3 coordinates antigen presentation, endothelial stability, and cholesterol metabolism to suppress hepatocellular carcinoma progression.The Journal of biological chemistry · 2026Article
- The impact of nationwide folic acid fortification on genetic variants associated with conotruncal heart defects.Research square · 2026Article
- Retinol dehydrogenase 10-mediated retinoic acid signaling regulates the neural crest cell microenvironment during enteric nervous system formation.Human molecular genetics · 2026Article
- Consuming your colors: carotenoid and retinol availability affects expression of color related genes in the mimic poison frog (Ranitomeya imitator).BMC genomics · 2025Article
- Amino acid insufficiency impairs hepatic vitamin A mobilization in mice.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Deep learning the dynamic regulatory sequence code of cardiac organoid differentiation.bioRxiv : the preprint server for biology · 2025Article
- Retinoic acid signaling and metabolism in heart failure.American journal of physiology. Heart and circulatory physiology · 2025Review
- Feedback regulation of retinaldehyde reductase DHRS3, a critical determinant of retinoic acid homeostasis.FEBS letters · 2025Article
- Identification and characterization of short-chain dehydrogenase/reductase 3 (DHRS3) deficiency, a retinoic acid embryopathy of humans.Genetics in medicine open · 2025Article
- Vitamin A supply in the eye and establishment of the visual cycle.Current topics in developmental biology · 2025Review
- Rewiring of the epigenome and chromatin architecture by exogenously induced retinoic acid signaling during zebrafish embryonic development.Nucleic acids research · 2024Article
- From phenotype to mechanism: Prenatal spectrum of NKAP mutation-related disorder and its pathogenesis inducing congenital heart disease.Journal of cellular and molecular medicine · 2024Article
- The etiology of congenital diaphragmatic hernia: the retinoid hypothesis 20 years later.Pediatric research · 2024Review
- Nephron progenitors rhythmically alternate between renewal and differentiation phases that synchronize with kidney branching morphogenesis.bioRxiv : the preprint server for biology · 2024Article
- Exploring the association between dietary vitamin A and coronary artery disease risk in men and women: findings from a US population study.Frontiers in nutrition · 2024Article
- Anti-tumor activity of all-trans retinoic acid in gastric-cancer: gene-networks and molecular mechanisms.Journal of experimental & clinical cancer research : CR · 2023Article
- Notch and retinoic acid signals regulate macrophage formation from endocardium downstream of Nkx2-5.Nature communications · 2023Article
- Hif1α/Dhrs3a Pathway Participates in Lipid Droplet Accumulation via Retinol and Ppar-γ in Fish Hepatocytes.International journal of molecular sciences · 2023Article
28 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Oxidation of retinol via retinaldehyde results in the formation of the essential morphogen all-trans-retinoic acid (ATRA). Previous studies have identified critical roles in the regulation of embryonic ATRA levels for retinol, retinaldehyde, and ATRA-oxidizing enzymes; however, the contribution of retinaldehyde reductases to ATRA metabolism is not completely understood. Herein, we investigate the role of the retinaldehyde reductase Dhrs3 in embryonic retinoid metabolism using a Dhrs3-deficient mouse. Lack of DHRS3 leads to a 40% increase in the levels of ATRA and a 60% and 55% decrease in the levels of retinol and retinyl esters, respectively, in Dhrs3(-/-) embryos compared to wild-type littermates. Furthermore, accumulation of excess ATRA is accompanied by a compensatory 30-50% reduction in the expression of ATRA synthetic genes and a 120% increase in the expression of the ATRA catabolic enzyme Cyp26a1 in Dhrs3(-/-) embryos vs. controls. Excess ATRA also leads to alterations (40-80%) in the expression of several developmentally important ATRA target genes. Consequently, Dhrs3(-/-) embryos die late in gestation and display defects in cardiac outflow tract formation, atrial and ventricular septation, skeletal development, and palatogenesis. These data demonstrate that the reduction of retinaldehyde by DHRS3 is critical for preventing formation of excess ATRA during embryonic development.
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