ArticleThe American journal of pathology2015
Transient receptor potential vanilloid 1 gene deficiency ameliorates hepatic injury in a mouse model of chronic binge alcohol-induced alcoholic liver disease.
Article in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73).BMJ (Clinical research ed.) · 2016Pooled it
- GPAM mediates mitochondrial dysfunction and the progression of alcoholic liver disease through lipid remodeling.Science advances · 2026Article
- Hepatic TRPC3 loss contributes to chronic alcohol consumption-induced hepatic steatosis and liver injury in mice.Life metabolism · 2024Article
- Hepatic Transcriptome and Its Regulation Following Soluble Epoxide Hydrolase Inhibition in Alcohol-Associated Liver Disease.The American journal of pathology · 2024Article
- Role of TRP Channels in Liver-Related Diseases.International journal of molecular sciences · 2023Review
- Expression and functions of transient receptor potential channels in liver diseases.Acta pharmaceutica Sinica. B · 2023Review
- The Preliminary Results for Evaluating Cocoa Butter's Hepatoprotective Effects against Lipid Accumulation and Inflammation in Adult Male Rats Chronically Fed Ethanol.Bioengineering (Basel, Switzerland) · 2022Article
- Review
- Comprehensive lipidomics reveals phenotypic differences in hepatic lipid turnover in ALD and NAFLD during alcohol intoxication.JHEP reports : innovation in hepatology · 2021Article
- Feeding mice a diet high in oxidized linoleic acid metabolites does not alter liver oxylipin concentrations.Prostaglandins, leukotrienes, and essential fatty acids · 2021Article
- Effects of diets enriched in linoleic acid and its peroxidation products on brain fatty acids, oxylipins, and aldehydes in mice.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018Article
- Reactive metabolites of acetaminophen activate and sensitize the capsaicin receptor TRPV1.Scientific reports · 2017Article
- Dietary Linoleic Acid and Its Oxidized Metabolites Exacerbate Liver Injury Caused by Ethanol via Induction of Hepatic Proinflammatory Response in Mice.The American journal of pathology · 2017Article
- Animal Models of Alcoholic Liver Disease: Pathogenesis and Clinical Relevance.Gene expression · 2017Review
- Osteopontin facilitates West Nile virus neuroinvasion via neutrophil "Trojan horse" transport.Scientific reports · 2017Article
- Occupational exposures at a polyvinyl chloride production facility are associated with significant changes to the plasma metabolome.Toxicology and applied pharmacology · 2016Article
- Dysregulation of hepatic cAMP levels via altered Pde4b expression plays a critical role in alcohol-induced steatosis.The Journal of pathology · 2016Article
- Aberrant post-translational protein modifications in the pathogenesis of alcohol-induced liver injury.World journal of gastroenterology · 2016Review
- Alcoholic Liver Disease: Update on the Role of Dietary Fat.Biomolecules · 2016Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Experimental alcohol-induced liver injury is exacerbated by a high polyunsaturated fat diet rich in linoleic acid. We postulated that bioactive oxidized linoleic acid metabolites (OXLAMs) play a critical role in the development/progression of alcohol-mediated hepatic inflammation and injury. OXLAMs are endogenous ligands for transient receptor potential vanilloid 1 (TRPV1). Herein, we evaluated the role of signaling through TRPV1 in an experimental animal model of alcoholic liver disease (ALD). Chronic binge alcohol administration increased plasma OXLAM levels, specifically 9- and 13-hydroxy-octadecadienoic acids. This effect was associated with up-regulation of hepatic TRPV1. Exposure of hepatocytes to these OXLAMs in vitro resulted in activation of TRPV1 signal transduction with increased intracellular Ca(2+) levels. Genetic depletion of TRPV1 did not blunt hepatic steatosis caused by ethanol, but prevented hepatic injury. TRPV1 deficiency protected from hepatocyte death and prevented the increase in proinflammatory cytokine and chemokine expression, including tumor necrosis factor-α, IL-6, macrophage inflammatory protein-2, and monocyte chemotactic protein 1. TRPV1 depletion markedly blunted ethanol-mediated induction of plasminogen activator inhibitor-1, an important alcohol-induced hepatic inflammation mediator, via fibrin accumulation. This study indicates, for the first time, that TRPV1 receptor pathway may be involved in hepatic inflammatory response in an experimental animal model of ALD. TRPV1-OXLAM interactions appear to play a significant role in hepatic inflammation/injury, further supporting an important role for dietary lipids in ALD.
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