ArticleNature communications2017
Hepatic p63 regulates steatosis via IKKβ/ER stress.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 47 citations in OpenAlex.
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- p63 controls metabolic activation of hepatic stellate cells and fibrosis via an HER2-ACC1 pathway.Cell reports. Medicine · 2024Article
- Rab18 Drift in Lipid Droplet and Endoplasmic Reticulum Interactions of Adipocytes under Obesogenic Conditions.International journal of molecular sciences · 2023Article
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- Protective Effects ofInternational journal of molecular sciences · 2023Article
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- Targeted therapeutics and novel signaling pathways in non-alcohol-associated fatty liver/steatohepatitis (NAFL/NASH).Signal transduction and targeted therapy · 2022Review
- Hepatic MDM2 Causes Metabolic Associated Fatty Liver Disease by Blocking Triglyceride-VLDL Secretion via ApoB Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- O-GlcNAcylated p53 in the liver modulates hepatic glucose production.Nature communications · 2021Article
- Fructose Causes Liver Damage, Polyploidy, and Dysplasia in the Setting of Short Telomeres and p53 Loss.Metabolites · 2021Article
- Spinal motor neuron loss occurs through a p53-and-p21-independent mechanism in the SmnExperimental neurology · 2021Article
- Genome-wide RNA interference screening reveals a COPI-MAP2K3 pathway required for YAP regulation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Liver osteopontin is required to prevent the progression of age-related nonalcoholic fatty liver disease.Aging cell · 2020Article
- Transcriptional Regulation in Non-Alcoholic Fatty Liver Disease.Metabolites · 2020Review
- Targeting Hepatic Glutaminase 1 Ameliorates Non-alcoholic Steatohepatitis by Restoring Very-Low-Density Lipoprotein Triglyceride Assembly.Cell metabolism · 2020Article
- miR-873-5p targets mitochondrial GNMT-Complex II interface contributing to non-alcoholic fatty liver disease.Molecular metabolism · 2019Article
- Deficiency of Mitochondrial Glycerol 3-Phosphate Dehydrogenase Contributes to Hepatic Steatosis.Hepatology (Baltimore, Md.) · 2019Article
- Liver-target nanotechnology facilitates berberine to ameliorate cardio-metabolic diseases.Nature communications · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
27 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p53 family members control several metabolic and cellular functions. The p53 ortholog p63 modulates cellular adaptations to stress and has a major role in cell maintenance and proliferation. Here we show that p63 regulates hepatic lipid metabolism. Mice with liver-specific p53 deletion develop steatosis and show increased levels of p63. Down-regulation of p63 attenuates liver steatosis in p53 knockout mice and in diet-induced obese mice, whereas the activation of p63 induces lipid accumulation. Hepatic overexpression of N-terminal transactivation domain TAp63 induces liver steatosis through IKKβ activation and the induction of ER stress, the inhibition of which rescues the liver functions. Expression of TAp63, IKKβ and XBP1s is also increased in livers of obese patients with NAFLD. In cultured human hepatocytes, TAp63 inhibition protects against oleic acid-induced lipid accumulation, whereas TAp63 overexpression promotes lipid storage, an effect reversible by IKKβ silencing. Our findings indicate an unexpected role of the p63/IKKβ/ER stress pathway in lipid metabolism and liver disease.
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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.