ArticleFEBS letters2025
Feedback regulation of retinaldehyde reductase DHRS3, a critical determinant of retinoic acid homeostasis.
Article in FEBS letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- The retinol-metabolizing enzyme DHRS3 coordinates antigen presentation, endothelial stability, and cholesterol metabolism to suppress hepatocellular carcinoma progression.The Journal of biological chemistry · 2026Article
- Discovery of a novel Nrf2 activator that modulates mitochondrial function in neurons by regulating DHRS3-Nrf2 interaction after ischemic stroke.Theranostics · 2026Article
- Identification of immunometabolism-associated genes and immune infiltration in sepsis-induced cardiomyopathy using integrated bioinformatics and machine learning approaches.The Journal of international medical research · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Retinoic acid is crucial for vertebrate embryogenesis, influencing anterior-posterior patterning and organogenesis through its interaction with nuclear hormone receptors comprising heterodimers of retinoic acid receptors (RARα, β, or γ) and retinoid X receptors (RXRα, β, or γ). Tissue retinoic acid levels are tightly regulated since both its excess and deficiency are deleterious. Dehydrogenase/reductase 3 (DHRS3) plays a critical role in this regulation by converting retinaldehyde to retinol, preventing excessive retinoic acid formation. Mutations in DHRS3 can result in embryonic lethality and congenital defects. This study shows that mouse Dhrs3 expression is responsive to vitamin A status and is directly regulated by the RAR/RXR complex through cis-regulatory elements. This highlights a negative feedback mechanism that ensures retinoic acid homeostasis.
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Registered trials
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