ArticleHepatology (Baltimore, Md.)2013
Aging promotes the development of diet-induced murine steatohepatitis but not steatosis.
Article in Hepatology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 124 citations in OpenAlex.
- Unveiling the role of age in MASLD development and biological process activation: Implications for translational research.Journal of physiology and biochemistry · 2026Article
- SIRT6-Mediated Deacetylation of ATF3 Promotes Silica-Induced Lung Fibrosis by Enhancing its Nuclear Import via Binding to Importin α.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Rapamycin Reverses the Hepatic Response to Diet-Induced Metabolic Stress That Is Amplified by Aging.Aging cell · 2026Article
- Dual roles of immunosenescence in cancer immunotherapy.Frontiers in immunology · 2026Review
- Review
- Role of cellular senescence in hepatic diseases (Review).International journal of molecular medicine · 2025Review
- Adipose tissue aging as a risk factor for metabolic organ abnormalities: mechanistic insights and the role of exercise interventions.Lipids in health and disease · 2025Review
- Macrophages: Subtypes, Distribution, Polarization, Immunomodulatory Functions, and Therapeutics.MedComm · 2025Review
- Aging and metabolic dysfunction-associated steatotic liver disease: a bidirectional relationship.Frontiers of medicine · 2025Review
- Delaying liver aging: Analysis of structural and functional alterations.World journal of gastroenterology · 2025Article
- Hepatic-specific vitamin D receptor downregulation alleviates aging-related metabolic dysfunction-associated steatotic liver disease.World journal of gastroenterology · 2025Article
- Aging immunity: unraveling the complex nexus of diet, gut microbiome, and immune function.Immunometabolism (Cobham, Surrey) · 2025Review
- [Advances in inflammaging in liver disease].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025Review
- Nucleic acid vaccines: innovations, efficacy, and applications in at-risk populations.Frontiers in immunology · 2025Review
- The infection-microbiome-immunity axis in bladder cancer: mechanistic insights and therapeutic perspectives.Frontiers in immunology · 2025Review
- Immunosenescence, Physical Exercise, and their Implications in Tumor Immunity and Immunotherapy.International journal of biological sciences · 2025Review
- The crosstalk between senescence, tumor, and immunity: molecular mechanism and therapeutic opportunities.MedComm · 2025Review
- Cell senescence in liver diseases: pathological mechanism and theranostic opportunity.Nature reviews. Gastroenterology & hepatology · 2024Review
- Ameliorative effect of bofutsushosan (Fangfengtongshengsan) extract on the progression of aging-induced obesity.Journal of natural medicines · 2024Article
- Macrophage senescence in health and diseases.Acta pharmaceutica Sinica. B · 2024Review
19 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
unlabelledThe prevalence of the metabolic syndrome and nonalcoholic fatty liver disease (NAFLD) in humans increases with age. It is unknown whether this association is secondary to the increased incidence of risk factors for NAFLD that occurs with aging, reflects the culmination of years of exposure to lifestyle factors such as a high-fat diet (HFD), or results from physiological changes that characterize aging. To examine this question, the development of NAFLD in response to a fixed period of HFD feeding was examined in mice of different ages. Mice aged 2, 8, and 18 months were fed 16 weeks of a low-fat diet or HFD. Increased body mass and insulin insensitivity occurred in response to HFD feeding irrespective of the age of the mice. The amount of HFD-induced hepatic steatosis as determined biochemically and histologically was also equivalent among the three ages. Liver injury occurred exclusively in the two older ages as reflected by increased serum alanine aminotransferase levels, positive terminal deoxynucleotide transferase-mediated deoxyuridine triphosphate nick end-labeling, and caspase activation. Older mice also had an elevated innate immune response with a more pronounced polarization of liver and adipose tissue macrophages into an M1 phenotype. Studies of cultured hepatocytes from young and old mice revealed that aged cells were selectively sensitized to the Fas death pathway.
conclusionAging does not promote the development of hepatic steatosis but leads to increased hepatocellular injury and inflammation that may be due in part to sensitization to the Fas death pathway and increased M1 macrophage polarization.
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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.