ArticleHepatology (Baltimore, Md.)2015
Osteopontin deficiency does not prevent but promotes alcoholic neutrophilic hepatitis in mice.
Article in Hepatology (Baltimore, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 116 citations in OpenAlex.
- Hepatoprotective effects of resolvin D1 in mice exposed to ethanol and galactosamine.Hepatology communications · 2026Article
- Therapeutics for Alcohol-Associated Liver Disease.Annual review of pharmacology and toxicology · 2026Review
- Oxidative Stress and Alcohol-Related Hepatitis: A Role for Future Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- An Update on Animal Models of Alcohol-Associated Liver Disease.The American journal of pathology · 2026Review
- Osteopontin: a central hub in the pathogenesis and therapeutic intervention of liver disease.Annals of medicine · 2025Review
- Immunological mechanisms and emerging therapeutic targets in alcohol-associated liver disease.Cellular & molecular immunology · 2025Review
- Characterizing Kupffer Cell Production of CD5 Antigen-Like and Its Function on Regulating Migration of Natural Killer T Cells.The American journal of pathology · 2025Article
- Activation of intestinal endogenous retroviruses by alcohol exacerbates liver disease.The Journal of clinical investigation · 2025Article
- Phytochemicals Targeting Inflammatory Pathways in Alcohol-Induced Liver Disease: A Mechanistic Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Immunology and treatments of fatty liver disease.Archives of toxicology · 2025Review
- Osteopontin: an indispensable component in common liver, pancreatic, and biliary related disease.Journal of cancer research and clinical oncology · 2024Review
- Article
- GSDMD induces hepatocyte pyroptosis to trigger alcoholic hepatitis through modulating mitochondrial dysfunction.Cell division · 2024Article
- Alcohol-associated liver disease.The Journal of clinical investigation · 2024Review
- Hepatocyte-specific mitogen-activated protein kinase phosphatase 1 in sexual dimorphism and susceptibility to alcohol induced liver injury.Frontiers in immunology · 2024Article
- Experimental In Vivo Toxicity Models for Alcohol Toxicity.The Eurasian journal of medicine · 2023Article
- Dysregulated Cyclic Nucleotide Metabolism in Alcohol-Associated Steatohepatitis: Implications for Novel Targeted Therapies.Biology · 2023Article
- Amelioration of ethanol-induced oxidative stress and alcoholic liver disease byActa pharmaceutica Sinica. B · 2023Article
- Research Progress of Pyroptosis in Fatty Liver Disease.International journal of molecular sciences · 2023Review
- Lactoferrin, Osteopontin and Lactoferrin-Osteopontin Complex: A Critical Look on Their Role in Perinatal Period and Cardiometabolic Disorders.Nutrients · 2023Review
23 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledAlcoholic hepatitis (AH) is a distinct spectrum of alcoholic liver disease (ALD) with intense neutrophilic (polymorphonuclear; PMN) inflammation and high mortality. Although a recent study implicates osteopontin (SPP1) in AH, SPP1 is also shown to have protective effects on experimental ALD. To address this unsettled question, we examined the effects of SPP1 deficiency in male mice given 40% calories derived from ad libitum consumption of the Western diet high in cholesterol and saturated fat and the rest from intragastric feeding of alcohol diet without or with weekly alcohol binge. Weekly binge in this new hybrid feeding model shifts chronic ASH with macrophage inflammation and perisinusoidal and pericellular fibrosis to AH in 57% (15 of 26) of mice, accompanied by inductions of chemokines (Spp1, Cxcl1, and interleukin [Il]-17a), progenitor genes (Cd133, Cd24, Nanog, and epithelial cell adhesion molecule), PMN infiltration, and clinical features of AH, such as hypoalbuminemia, bilirubinemia, and splenomegaly. SPP1 deficiency does not reduce AH incidence and inductions of progenitor and fibrogenic genes, but rather enhances the Il-17a induction and PMN infiltration in some mice. Furthermore, in the absence of SPP1, chronic ASH mice without weekly binge begin to develop AH.
conclusionThese results suggest that SPP1 has a protective, rather than causal, role for experimental AH reproduced in our model.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.