ArticleHepatology (Baltimore, Md.)2020
Protective and Detrimental Roles of p38α Mitogen-Activated Protein Kinase in Different Stages of Nonalcoholic Fatty Liver Disease.
Article in Hepatology (Baltimore, Md.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Immune Activation in Primary Sclerosing Cholangitis: A Systematic Review and Comparative Analysis With Inflammatory Bowel Diseases.United European gastroenterology journal · 2025Pooled it
- Hepatic steatosis affects the outcome of anti-tuberculosis treatment in pulmonary tuberculosis patients.Journal of clinical tuberculosis and other mycobacterial diseases · 2026Article
- Chemokines and chemokine receptors in metabolic dysfunction-associated steatohepatitis: pathogenic mechanisms and clinical implications.Cellular & molecular biology letters · 2026Review
- SHANK3 Deficiency in AgRP Neurons Inhibits Diet-Induced Obesity by Activating p38α.Neuroscience bulletin · 2026Article
- Immune crosstalk in metabolic dysfunction-associated steatotic liver disease: interactions between innate and adaptive immunity.Frontiers in immunology · 2026Review
- Immunopathogenic mechanisms and immunoregulatory therapies in MASLD.Cellular & molecular immunology · 2025Review
- Infiltrating macrophages replace Kupffer cells and play diverse roles in severe alcohol-associated hepatitis.Cellular & molecular immunology · 2025Article
- p38α MAPK Regulation of Energy Metabolism in Skeletal Muscle Offers a Therapeutic Path for Type 2 Diabetes.Cells · 2025Review
- AAV8-mediated silencing of Atad3 prevents the progression from simple steatosis to MASH in mice by reduced IL6 secretion.Biochimica et biophysica acta. Molecular basis of disease · 2025Article
- Phytochemicals Targeting Inflammatory Pathways in Alcohol-Induced Liver Disease: A Mechanistic Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The SIRT6 Activator MDL-800 Inhibits PPARα and Fatty acid Oxidation-Related Gene Expression in Hepatocytes.Biomolecules & therapeutics · 2025Article
- New therapeutic target for alcohol-associated hepatitis (AH): AH-associated IL-8eGastroenterology · 2024Article
- Shank3 deficiency elicits autistic-like behaviors by activating p38α in hypothalamic AgRP neurons.Molecular autism · 2024Article
- Obesogenic Diet in Mice Leads to Inflammation and Oxidative Stress in the Mother in Association with Sex-Specific Changes in Fetal Development, Inflammatory Markers and Placental Transcriptome.Antioxidants (Basel, Switzerland) · 2024Article
- Mitochondria- and NOX4-dependent antioxidant defense mitigates progression to nonalcoholic steatohepatitis in obesity.The Journal of clinical investigation · 2023Article
- Overexpression of Interleukin-8 Promotes the Progression of Fatty Liver to Nonalcoholic Steatohepatitis in Mice.International journal of molecular sciences · 2023Article
- Integrated strategy of RNA-sequencing and network pharmacology for exploring the protective mechanism of Shen-Shi-Jiang-Zhuo formula in rat with non-alcoholic fatty liver disease.Pharmaceutical biology · 2022Article
- Mechanism and Therapeutic Targets of c-Jun-N-Terminal Kinases Activation in Nonalcoholic Fatty Liver Disease.Biomedicines · 2022Review
- Burmese pythons exhibit a transient adaptation to nutrient overload that prevents liver damage.The Journal of general physiology · 2022Article
- Immune-related pathogenesis and therapeutic strategies of nonalcoholic steatohepatitis.Archives of pharmacal research · 2022Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND AND
aimsNeutrophil infiltration is a hallmark of nonalcoholic steatohepatitis (NASH), but how this occurs during the progression from steatosis to NASH remains obscure. Human NASH features hepatic neutrophil infiltration and up-regulation of major neutrophil-recruiting chemokines (e.g., chemokine [C-X-C motif] ligand 1 [CXCL1] and interleukin [IL]-8). However, mice fed a high-fat diet (HFD) only develop fatty liver without significant neutrophil infiltration or elevation of chemokines. The aim of this study was to determine why mice are resistant to NASH development and the involvement of p38 mitogen-activated protein kinase (p38) activated by neutrophil-derived oxidative stress in the pathogenesis of NASH. APPROACH AND
resultsInflamed human hepatocytes attracted neutrophils more effectively than inflamed mouse hepatocytes because of the greater induction of CXCL1 and IL-8 in human hepatocytes. Hepatic overexpression of Cxcl1 and/or IL-8 promoted steatosis-to-NASH progression in HFD-fed mice by inducing liver inflammation, injury, and p38 activation. Pharmacological inhibition of p38α/β or hepatocyte-specific deletion of p38a (a predominant form in the liver) attenuated liver injury and fibrosis in the HFD
conclusionsGenetic ablation of hepatic p38a increases simple steatosis but ameliorates oxidative stress-driven NASH, indicating that p38α plays distinct roles depending on the disease stages, which may set the stage for investigating p38α as a therapeutic target for the treatment of NASH.
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Registered trials
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.