ArticleAtherosclerosis2012
Hepatocyte-specific IKKβ expression aggravates atherosclerosis development in APOE*3-Leiden mice.
Article in Atherosclerosis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 40 citations in OpenAlex.
- Unconventional mechanisms of resveratrol in atherosclerosis prevention and management.World journal of experimental medicine · 2026Review
- Lipid overload meets S-palmitoylation: a metabolic signalling nexus driving cardiovascular and heart disease.Cell communication and signaling : CCS · 2025Review
- White Tea Reduces Dyslipidemia, Inflammation, and Oxidative Stress in the Aortic Arch in a Model of Atherosclerosis Induced by Atherogenic Diet in ApoE Knockout Mice.Pharmaceuticals (Basel, Switzerland) · 2024Article
- DHCR24 inhibitor SH42 increases desmosterol without preventing atherosclerosis development in mice.iScience · 2024Article
- Atherosclerosis: an overview of mouse models and a detailed methodology to quantify lesions in the aortic root.Vascular biology (Bristol, England) · 2024Review
- Identification of common signature genes and pathways underlying the pathogenesis association between nonalcoholic fatty liver disease and atherosclerosis.Frontiers in cardiovascular medicine · 2023Article
- HIV Protein Tat Induces Macrophage Dysfunction and Atherosclerosis Development in Low-Density Lipoprotein Receptor-Deficient Mice.Cardiovascular drugs and therapy · 2022Article
- Pharmacological treatment with FGF21 strongly improves plasma cholesterol metabolism to reduce atherosclerosis.Cardiovascular research · 2022Article
- Fibroblast-specific IKK-β deficiency ameliorates angiotensin II-induced adverse cardiac remodeling in mice.JCI insight · 2021Article
- Colesevelam enhances the beneficial effects of brown fat activation on hyperlipidaemia and atherosclerosis development.Cardiovascular research · 2020Article
- Dare to Compare. Development of Atherosclerotic Lesions in Human, Mouse, and Zebrafish.Frontiers in cardiovascular medicine · 2020Review
- Intermittent hypoxia and hypercapnia induces inhibitor of nuclear factor-κB kinase subunit β-dependent atherosclerosis in pulmonary arteries.American journal of physiology. Regulatory, integrative and comparative physiology · 2019Article
- Deficiency of Adipocyte IKKβ Affects Atherosclerotic Plaque Vulnerability in Obese LDLR Deficient Mice.Journal of the American Heart Association · 2019Article
- Dietary Mannan Oligosaccharides Modulate Gut Microbiota, Increase Fecal Bile Acid Excretion, and Decrease Plasma Cholesterol and Atherosclerosis Development.Molecular nutrition & food research · 2018Article
- Chronic intermittent hypoxia exposure-induced atherosclerosis: a brief review.Immunologic research · 2015Review
- Brown fat activation reduces hypercholesterolaemia and protects from atherosclerosis development.Nature communications · 2015Article
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveThe liver is the key organ involved in systemic inflammation, but the relation between hepatic inflammation and atherogenesis is poorly understood. Since nuclear factor-κB (NF-κB) is a central regulator of inflammatory processes, we hypothesized that chronically enhanced hepatic NF-κB activation, through hepatocyte-specific expression of IκB kinase-β (IKKβ) (LIKK), will aggravate atherosclerosis development in APOE*3-Leiden (E3L) mice. METHODS AND
resultsE3L.LIKK and E3L control littermates were fed a Western-type diet for 24 weeks. E3L.LIKK mice showed a 2.3-fold increased atherosclerotic lesion area and more advanced atherosclerosis in the aortic root with less segments without atherosclerotic lesions (11% vs. 42%), and more segments with mild (63% vs. 44%) and severe (26% vs. 14%) lesions. Expression of LIKK did not affect basal levels of inflammatory parameters, but plasma cytokine levels tended to be higher in E3L.LIKK mice after lipopolysaccharide (LPS) administration. E3L.LIKK mice showed transiently increased plasma cholesterol levels, confined to (V)LDL. This transient character resulted in a mild (+17%) increased cumulative plasma cholesterol exposure.
conclusionWe conclude that selective activation of NF-κB in hepatocytes considerably promotes atherosclerosis development which is (at least partly) explained by an increased sensitivity to proinflammatory triggers and transiently increased plasma cholesterol levels.
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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.