ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2015
Increased 4-hydroxynonenal protein adducts in male GSTA4-4/PPAR-α double knockout mice enhance injury during early stages of alcoholic liver disease.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- NOX-NOS crosstalk in the liver-brain axis: Novel insights for redox regulation and neurodegenerative diseases.Redox biology · 2025Review
- Causal Gene Identification and Biomarker Prioritization in Periodontitis via Integrative Multiomics and Mendelian Randomization.Mediators of inflammation · 2025Article
- iTRAQ Quantitative Proteomic Analysis of Different Expressed Proteins and Signal Pathways in Bakuchiol-Induced Hepatotoxicity.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury.Experimental & molecular medicine · 2021Review
- Huanglian Jiedu Decoction in the Treatment of the Traditional Chinese Medicine Syndrome "Shanghuo"-An Intervention Study.Frontiers in pharmacology · 2021Article
- Alcoholic hepatitis and metabolic disturbance in female mice: a more tractable model thanDisease models & mechanisms · 2020Article
- Lipid peroxidation derived reactive aldehydes in alcoholic liver disease.Current opinion in toxicology · 2019Article
- Publisher Correction: The gut-liver axis and the intersection with the microbiome.Nature reviews. Gastroenterology & hepatology · 2018Article
- Knockout of the Gsta4 Gene in Male Mice Leads to an Altered Pattern of Hepatic Protein Carbonylation and Enhanced Inflammation Following Chronic Consumption of an Ethanol Diet.Alcoholism, clinical and experimental research · 2018Article
- The gut-liver axis and the intersection with the microbiome.Nature reviews. Gastroenterology & hepatology · 2018Review
- Role of Nutrition in Alcoholic Liver Disease: Summary of the Symposium at the ESBRA 2017 Congress.Biomolecules · 2018Article
- Dysregulation of antioxidant responses in patients diagnosed with concomitant Primary Sclerosing Cholangitis/Inflammatory Bowel Disease.Experimental and molecular pathology · 2018Article
- Global Deletion of Glutathione S-Transferase A4 Exacerbates Developmental Nonalcoholic Steatohepatitis.The American journal of pathology · 2017Article
- Danshen protects against early-stage alcoholic liver disease in mice via inducing PPARα activation and subsequent 4-HNE degradation.PloS one · 2017Article
- Pathogenesis of Alcoholic Liver Disease.Clinics in liver disease · 2016Review
- Aberrant post-translational protein modifications in the pathogenesis of alcohol-induced liver injury.World journal of gastroenterology · 2016Review
- Deletion of GSTA4-4 results in increased mitochondrial post-translational modification of proteins by reactive aldehydes following chronic ethanol consumption in mice.Redox biology · 2016Article
- Article
- The Genetic Architecture of Murine Glutathione Transferases.PloS one · 2016Article
- Increased hepatocellular protein carbonylation in human end-stage alcoholic cirrhosis.Free radical biology & medicine · 2015Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
To test the significance of lipid peroxidation in the development of alcoholic liver injury, an ethanol (EtOH) liquid diet was fed to male 129/SvJ mice (wild-type, WT) and glutathione S-transferase A4-4-null (GSTA4-/-) mice for 40 days. GSTA4-/- mice were crossed with peroxisome proliferator-activated receptor-α-null mice (PPAR-α-/-), and the effects of EtOH in the resulting double knockout (dKO) mice were compared with the other strains. EtOH increased lipid peroxidation in all except WT mice (P < 0.05). Increased steatosis and mRNA expression of the inflammatory markers CXCL2, tumor necrosis factor-α (TNF-α), and α-smooth muscle actin (α-SMA) were observed in EtOH GSTA4-/- compared with EtOH WT mice (P < 0.05). EtOH PPAR-α-/- mice had increased steatosis, serum alanine aminotransferase (ALT), and hepatic CD3+ T cell populations and elevated mRNA encoding CD14, CXCL2, TNF-α, IL-6, CD138, transforming growth factor-β, platelet-derived growth factor receptor-β (PDGFR-β), matrix metalloproteinase (MMP)-9, MMP-13, α-SMA, and collagen type 1 compared with EtOH WT mice. EtOH-fed dKO mice displayed elevation of periportal hepatic 4-hydroxynonenal adducts and serum antibodies against malondialdehyde adducts compared with EtOH feeding of GSTA4-/-, PPAR-α-/-, and WT mice (P < 0.05). ALT was higher in EtOH dKO mice compared with all other groups (P < 0.001). EtOH-fed dKO mice displayed elevated mRNAs for TNF-α and CD14, histological evidence of fibrosis, and increased PDGFR, MMP-9, and MMP-13 mRNAs compared with the EtOH GSTA4-/- or EtOH PPAR-α-/- genotype (P < 0.05). These findings demonstrate the central role lipid peroxidation plays in mediating progression of alcohol-induced necroinflammatory liver injury, stellate cell activation, matrix remodeling, and fibrosis.
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