ArticleHepatology (Baltimore, Md.)2014
Alcohol dehydrogenase III exacerbates liver fibrosis by enhancing stellate cell activation and suppressing natural killer cells in mice.
Article in Hepatology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 67 citations in OpenAlex.
- Dynamic crosstalk between HSCs and liver microenvironment: multicellular interactions in the regulation of liver fibrosis.Frontiers in cell and developmental biology · 2025Review
- Class III Alcohol Dehydrogenase Plays a Key Role in the Onset of Alcohol-Related/-Associated Liver Disease as an S-Nitrosoglutathione Reductase in Mice.International journal of molecular sciences · 2023Article
- The Important Roles of Natural Killer Cells in Liver Fibrosis.Biomedicines · 2023Review
- Subclinical versus advanced forms of alcohol-related liver disease: Need for early detection.Clinical and molecular hepatology · 2023Review
- Effects of Gene Polymorphisms, Metabolic Activity, and Content of Alcohol Dehydrogenase and Acetaldehyde Dehydrogenases on Prognosis of Hepatocellular Carcinoma Patients.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2022Article
- The antifibrotic role of natural killer cells in liver fibrosis.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- The Role of Carnitine Orotate Complex in Fatty Liver.Diabetes & metabolism journal · 2021Article
- Extra- and Intra-Cellular Mechanisms of Hepatic Stellate Cell Activation.Biomedicines · 2021Review
- The Immune System through the Lens of Alcohol Intake and Gut Microbiota.International journal of molecular sciences · 2021Review
- Interleukin-10 Attenuates Liver Fibrosis Exacerbated by Thermoneutrality.Frontiers in medicine · 2021Article
- Possible Immunotherapeutic Strategies Based on Carcinogen-Dependent Subgroup Classification for Oral Cancer.Frontiers in molecular biosciences · 2021Review
- Intravital imaging of interactions between iNKT and kupffer cells to clear free lipids during steatohepatitis.Theranostics · 2021Article
- Recent advances of sterile inflammation and inter-organ cross-talk in alcoholic liver disease.Experimental & molecular medicine · 2020Review
- Functional Inhibition of Natural Killer Cells in a BALB/c Mouse Model of Liver Fibrosis Induced byFrontiers in cellular and infection microbiology · 2020Article
- Alcohol and multiple sclerosis: an immune system-based review.International journal of physiology, pathophysiology and pharmacology · 2020Review
- Review
- Ocular mucous membrane pemphigoid: a review.Immunologic research · 2019Review
- T-cell senescence contributes to abnormal glucose homeostasis in humans and mice.Cell death & disease · 2019Article
- "Let my liver rather heat with wine" - a review of hepatic fibrosis pathophysiology and emerging therapeutics.Hepatic medicine : evidence and research · 2019Article
- CXScientific reports · 2018Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
Abstract
unlabelledThe important roles of retinols and their metabolites have recently been emphasized in the interactions between hepatic stellate cells (HSCs) and natural killer (NK) cells. Nevertheless, the expression and role of retinol metabolizing enzyme in both cell types have yet to be clarified. Thus, we investigated the expression of retinol metabolizing enzyme and its role in liver fibrosis. Among several retinol metabolizing enzymes, only alcohol dehydrogenase (ADH) 3 expression was detected in isolated HSCs and NK cells, whereas hepatocytes express all of them. In vitro treatment with 4-methylpyrazole (4-MP), a broad ADH inhibitor, or depletion of the ADH3 gene down-regulated collagen and transforming growth factor-β1 (TGF-β1) gene expression, but did not affect α-smooth muscle actin gene expression in cultured HSCs. Additionally, in vitro, treatments with retinol suppressed NK cell activities, whereas inhibition of ADH3 enhanced interferon-γ (IFN-γ) production and cytotoxicity of NK cells against HSCs. In vivo, genetic depletion of the ADH3 gene ameliorated bile duct ligation- and carbon tetrachloride-induced liver fibrosis, in which a higher number of apoptotic HSCs and an enhanced activation of NK cells were detected. Freshly isolated HSCs from ADH3-deficient mice showed reduced expression of collagen and TGF-β1, but enhanced expression of IFN-γ was detected in NK cells from these mice compared with those of control mice. Using reciprocal bone marrow transplantation of wild-type and ADH3-deficient mice, we demonstrated that ADH3 deficiency in both HSCs and NK cells contributed to the suppressed liver fibrosis.
conclusionADH3 plays important roles in promoting liver fibrosis by enhancing HSC activation and inhibiting NK cell activity, and could be used as a potential therapeutic target for the treatment of liver fibrosis.
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