ArticleExperimental animals2018
Deletion of both p62 and Nrf2 spontaneously results in the development of nonalcoholic steatohepatitis.
Article in Experimental animals, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Intestinal epithelial cell-specific restoration of Nrf2 gene in whole-body-knockout mice ameliorates acute colitis.Experimental animals · 2025Article
- Article
- Specific targeting of the NRF2/β-TrCP axis promotes beneficial effects in NASH.Redox biology · 2024Article
- Article
- Identification and validation of potential diagnostic signature and immune cell infiltration for NAFLD based on cuproptosis-related genes by bioinformatics analysis and machine learning.Frontiers in immunology · 2023Article
- Nuclear factor erythroid 2-related factor 2-mediated signaling and metabolic associated fatty liver disease.World journal of gastroenterology · 2022Review
- Antioxidative Self-Assembling Nanoparticles Attenuate the Development of Steatohepatitis and Inhibit Hepatocarcinogenesis in Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Oxidative Stress Is a Key Modulator in the Development of Nonalcoholic Fatty Liver Disease.Antioxidants (Basel, Switzerland) · 2021Review
- Weight-loss-independent benefits of exercise on liver steatosis and stiffness in Japanese men with NAFLD.JHEP reports : innovation in hepatology · 2021Article
- Prevention of non-alcoholic steatohepatitis by long-term exercise via the induction of phenotypic changes in Kupffer cells of hyperphagic obese mice.Physiological reports · 2021Article
- Effects of Exercise on the Oral Microbiota and Saliva of Patients with Non-Alcoholic Fatty Liver Disease.International journal of environmental research and public health · 2021Article
- Gender difference in development of steatohepatitis in p62/Sqstm1 and Nrf2 double-knockout mice.Experimental animals · 2020Article
- Understanding lipotoxicity in NAFLD pathogenesis: is CD36 a key driver?Cell death & disease · 2020Review
- A low glycemic diet protects disease-prone Nrf2-deficient mice against age-related macular degeneration.Free radical biology & medicine · 2020Article
- Molecular Mechanisms: Connections between Nonalcoholic Fatty Liver Disease, Steatohepatitis and Hepatocellular Carcinoma.International journal of molecular sciences · 2020Review
- Effects of a DPP4 Inhibitor on Progression of NASH-related HCC and the p62/ Keap1/Nrf2-Pentose Phosphate Pathway in a Mouse Model.Liver cancer · 2019Article
- In Utero Dexamethasone Exposure Exacerbates Hepatic Steatosis in Rats That Consume Fructose During Adulthood.Nutrients · 2019Article
- Tsumura-Suzuki obese diabetic mice-derived hepatic tumors closely resemble human hepatocellular carcinomas in metabolism-related genes expression and bile acid accumulation.Hepatology international · 2018Article
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic steatohepatitis (NASH) is one of the leading causes of chronic liver disease worldwide. However, details of pathogenetic mechanisms remain unknown. Deletion of both p62/Sqstm1 and Nrf2 genes spontaneously led to the development of NASH in mice fed a normal chow and was associated with liver tumorigenesis. The pathogenetic mechanism (s) underlying the NASH development was investigated in p62:Nrf2 double-knockout (DKO) mice. DKO mice showed massive hepatomegaly and steatohepatitis with fat accumulation and had hyperphagia-induced obesity coupled with insulin resistance and adipokine imbalance. They also showed dysbiosis associated with an increased proportion of gram-negative bacteria species and an increased lipopolysaccharide (LPS) level in feces. Intestinal permeability was elevated in association with both epithelial damage and decreased expression levels of tight junction protein zona occludens-1, and thereby LPS levels were increased in serum. For Kupffer cells, the foreign body phagocytic capacity was decreased in magnetic resonance imaging, and the proportion of M1 cells was increased in DKO mice. In vitro experiments showed that the inflammatory response was accelerated in the p62:Nrf2 double-deficient Kupffer cells when challenged with a low dose of LPS. Diet restriction improved the hepatic conditions of NASH in association with improved dysbiosis and decreased LPS levels. The results suggest that in DKO mice, activation of innate immunity by excessive LPS flux from the intestines, occurring both within and outside the liver, is central to the development of hepatic damage in the form of NASH.
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