ArticleFrontiers of medicine2019
Rdh13 deficiency weakens carbon tetrachloride-induced liver injury by regulating Spot14 and Cyp2e1 expression levels.
Article in Frontiers of medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- Identification of potential bladder cancer drug targets through Mendelian randomization and molecular docking.Discover oncology · 2025Article
- CYP2E1 deficit mediates cholic acid-induced malignant growth in hepatocellular carcinoma cells.Molecular medicine (Cambridge, Mass.) · 2024Article
- Regulating Retinoic Acid Availability during Development and Regeneration: The Role of the CYP26 Enzymes.Journal of developmental biology · 2020Review
- Generation of Retinaldehyde for Retinoic Acid Biosynthesis.Biomolecules · 2019Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrion-localized retinol dehydrogenase 13 (Rdh13) is a short-chain dehydrogenase/reductase involved in vitamin A metabolism in both humans and mice. We previously generated Rdh13 knockout mice and showed that Rdh13 deficiency causes severe acute retinal light damage. In this study, considering that Rdh13 is highly expressed in mouse liver, we further evaluated the potential effect of Rdh13 on liver injury induced by carbon tetrachloride (CCl
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Registered trials
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