ArticlePloS one2023
A new NASH model in aged mice with rapid progression of steatohepatitis and fibrosis.
Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Precision pathophysiology in steatotic liver disease.Clinical and molecular hepatology · 2026Review
- Unveiling the role of age in MASLD development and biological process activation: Implications for translational research.Journal of physiology and biochemistry · 2026Article
- Effectiveness of dietary modifications in reversing damage induced by high-fat diet in rats.Journal of physiology and biochemistry · 2026Article
- Comparison and Characteristics of MASLD Mouse Models.Biomedicines · 2026Review
- Metabolic dysfunction-associated steatotic liver disease and steatohepatitis-associated hepatocarcinoma preclinical models.Nature reviews. Gastroenterology & hepatology · 2026Review
- A mitochondrial amidoxime-reducing component 1 (mARC1) A168T amino acid substitution does not confer protection from MASH and fibrosis in multiple mouse models of chronic liver disease.The Biochemical journal · 2026Article
- TIPE2 deficiency amplifies inflammation and immune dysregulation in MASH through modulating hepatic lipid metabolism and immune cell function.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Article
- Butein Alleviates Non-Alcoholic Steatohepatitis in Leptin-Deficient Mice by Modulating the PDE4/cAMP/p-CREB Pathway.Drug design, development and therapy · 2025Article
- Complement 3a Receptor 1 on Macrophages and Kupffer cells is not required for the Pathogenesis of Metabolic Dysfunction-Associated Steatotic Liver Disease.medRxiv : the preprint server for health sciences · 2024Article
- The Potential Role of C-Reactive Protein in Metabolic-Dysfunction-Associated Fatty Liver Disease and Aging.Biomedicines · 2023Review
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Authors and funding
10 authors.
Funding
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Abstract
Non-alcoholic fatty liver disease (NAFLD) has a high prevalence worldwide, with a significant proportion of patients progressing into non-alcoholic steatohepatitis (NASH) and further into cirrhosis and hepatocellular carcinoma (HCC). Most of the current animal models of NASH have limitations, such as incompatibility with human pathogenesis characteristics or long induction periods, which severely limit the development of new drugs and preclinical studies for NASH. We investigated the progression of NASH and fibrosis, as well as metabolic indicators, at different time points in aged mice induced by the Gubra Amylin NASH (GAN) diet, a high-fat, high-sugar, high-cholesterol diet, and attempted to establish a rapid and useful mouse model of NASH. Young and aged C57BL/6 mice were induced on a normal chow or GAN diet for 12 and 21 weeks, respectively. After 12 weeks of induction, aged mice developed NASH, including hepatic steatosis, lobular inflammation and hepatic ballooning, and the phenotype was more severe compared with young mice. After 21 weeks of induction, aged mice developed hepatic fibrosis, which greatly shortened the induction time compared with young mice. Furthermore, analysis of immune cell infiltration in the liver by flow cytometry elucidated the changes of multiple immune cells during the pathogenesis of NASH. These findings suggest that aged mice may develop NASH and fibrosis more rapidly under GAN diet induction, which may significantly shorten the period for preclinical studies of NASH.
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