ArticleCell metabolism2016
Physiological Suppression of Lipotoxic Liver Damage by Complementary Actions of HDAC3 and SCAP/SREBP.
Article in Cell metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
49 citing papers in PubMed, 75 citations in OpenAlex.
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- Wheat Bran-Derived Zinc Phytate Mitigates Hepatic Inflammation and Metabolic Disorders Associated with Gut Microbiota-FXR-PGC-1α Signaling in High-Fat Diet-Fed C57BL/6J Mice.Foods (Basel, Switzerland) · 2025Article
- Dietary saturated fatty acids promote lung myeloid cell inflammasome activation and IL-1β-mediated inflammation in mice and humans.Science translational medicine · 2025Article
- HDAC3 in action: Expanding roles in inflammation and inflammatory diseases.Cell proliferation · 2025Review
- The Roles of White Adipose Tissue and Liver NADPH in Dietary Restriction-Induced Longevity.Antioxidants (Basel, Switzerland) · 2024Review
- Nuclear receptor corepressors non-canonically drive glucocorticoid receptor-dependent activation of hepatic gluconeogenesis.Nature metabolism · 2024Article
- Article
- mTORC1 controls murine postprandial hepatic glycogen synthesis via Ppp1r3b.The Journal of clinical investigation · 2024Article
- Identification of novel targets associated with cholesterol metabolism in nonalcoholic fatty liver disease: a comprehensive study using Mendelian randomization combined with transcriptome analysis.Frontiers in genetics · 2024Article
- Oxidative stress induces lysosomal membrane permeabilization and ceramide accumulation in retinal pigment epithelial cells.Disease models & mechanisms · 2023Article
- Cellular Alterations in Carbohydrate and Lipid Metabolism Due to Interactions with Nanomaterials.Journal of functional biomaterials · 2023Review
- Mechanisms of regulation of motility of the gastrointestinal tract and the hepatobiliary system under the chronic action of nanocolloids.Scientific reports · 2023Article
- Deacetylase-dependent and -independent role of HDAC3 in cardiomyopathy.Journal of cellular physiology · 2023Article
- In Vivo Two-Photon Imaging Analysis of Dynamic Degradation of Hepatic Lipid Droplets in MS-275-Treated Mouse Liver.International journal of molecular sciences · 2022Article
- Reprogramming of Hepatic Metabolism and Microenvironment in Nonalcoholic Steatohepatitis.Annual review of nutrition · 2022Review
- Inhibition of nonalcoholic fatty liver disease in mice by selective inhibition of mTORC1.Science (New York, N.Y.) · 2022Article
- Activation of Liver mTORC1 Protects Against NASH via Dual Regulation of VLDL-TAG Secretion and De Novo Lipogenesis.Cellular and molecular gastroenterology and hepatology · 2022Article
- Role of endothelial cells in pulmonary fibrosis via SREBP2 activation.JCI insight · 2021Article
- Genistein and exercise treatment reduced NASH related HDAC3, IL-13 and MMP-12 expressions in ovariectomized rats fed with high fat high fructose diet.Journal of traditional and complementary medicine · 2021Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Liver fat accumulation precedes non-alcoholic steatohepatitis, an increasing cause of end-stage liver disease. Histone deacetylase 3 (HDAC3) is required for hepatic triglyceride homeostasis, and sterol regulatory element binding protein (SREBP) regulates the lipogenic response to feeding, but the crosstalk between these pathways is unknown. Here we show that inactivation of SREBP by hepatic deletion of SREBP cleavage activating protein (SCAP) abrogates the increase in lipogenesis caused by loss of HDAC3, but fatty acid oxidation remains defective. This combination leads to accumulation of lipid intermediates and to an energy drain that collectively cause oxidative stress, inflammation, liver damage, and, ultimately, synthetic lethality. Remarkably, this phenotype is prevented by ectopic expression of nuclear SREBP1c, revealing a surprising benefit of de novo lipogenesis and triglyceride synthesis in preventing lipotoxicity. These results demonstrate that HDAC3 and SCAP control symbiotic pathways of liver lipid metabolism that are critical for suppression of lipotoxicity.
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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.