ArticlePloS one2010
ApoE-/- PGC-1α-/- mice display reduced IL-18 levels and do not develop enhanced atherosclerosis.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Single-cell and spatial transcriptomics map senescent vascular cells in arterial remodeling during atherosclerosis in mice.Nature aging · 2025Article
- Multi-modal transcriptomics: integrating machine learning and convolutional neural networks to identify immune biomarkers in atherosclerosis.Frontiers in cardiovascular medicine · 2024Article
- DPP4 inhibition impairs senohemostasis to improve plaque stability in atherosclerotic mice.The Journal of clinical investigation · 2023Article
- Mitochondrial Dysfunction in the Cardio-Renal Axis.International journal of molecular sciences · 2023Review
- Comprehensive Analysis of Mitochondrial Dynamics Alterations in Heart Diseases.International journal of molecular sciences · 2023Review
- Coronary microvascular injury in myocardial infarction: perception and knowledge for mitochondrial quality control.Theranostics · 2021Review
- Candidate SNP Markers of Atherogenesis Significantly Shifting the Affinity of TATA-Binding Protein for Human Gene Promoters show stabilizing Natural Selection as a Sum of Neutral Drift Accelerating Atherogenesis and Directional Natural Selection Slowing It.International journal of molecular sciences · 2020Article
- Oxidative Stress in Ischemic Heart Disease.Oxidative medicine and cellular longevity · 2020Review
- Hydroxytyrosol Ameliorates Endothelial Function under Inflammatory Conditions by Preventing Mitochondrial Dysfunction.Oxidative medicine and cellular longevity · 2018Article
- SAK-HV Triggered a Short-period Lipid-lowering Biotherapy Based on the Energy Model of Liver Proliferation via a Novel Pathway.Theranostics · 2017Article
- PGC-1α dictates endothelial function through regulation of eNOS expression.Scientific reports · 2016Article
- Role of PGC-1α in Vascular Regulation: Implications for Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2016Review
- PGC-1α Modulates Telomere Function and DNA Damage in Protecting against Aging-Related Chronic Diseases.Cell reports · 2015Article
- Endothelial PGC-1α mediates vascular dysfunction in diabetes.Cell metabolism · 2014Article
- Macrophage PPAR gamma Co-activator-1 alpha participates in repressing foam cell formation and atherosclerosis in response to conjugated linoleic acid.EMBO molecular medicine · 2013Article
- Peroxisome proliferator-activated receptor γ coactivator-1α is a central negative regulator of vascular senescence.Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- Mitochondria and endothelial function.Circulation research · 2013Review
- Aging and vascular dysfunction: beneficial melatonin effects.Age (Dordrecht, Netherlands) · 2013Article
- Atherosclerosis: an epigenetic balancing act that goes wrong.Current atherosclerosis reports · 2011Review
- Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAtherosclerosis is a chronic inflammatory disease that evolves from the interaction of activated endothelial cells, macrophages, lymphocytes and modified lipoproteins (LDLs). In the last years many molecules with crucial metabolic functions have been shown to prevent important steps in the progression of atherogenesis, including peroxisome proliferator activated receptors (PPARs) and the class III histone deacetylase (HDAC) SIRT1. The PPARγ coactivator 1 alpha (Ppargc1a or PGC-1α) was identified as an important transcriptional cofactor of PPARγ and is activated by SIRT1. The aim of this study was to analyze total PGC-1α deficiency in an atherosclerotic mouse model. METHODOLOGY/PRINCIPAL
findingsTo investigate if total PGC-1α deficiency affects atherosclerosis, we compared ApoE(-/-) PGC-1α(-/-) and ApoE(-/-) PGC-1α(+/+) mice kept on a high cholesterol diet. Despite having more macrophages and a higher ICAM-1 expression in plaques, ApoE(-/-) PGC-1α(-/-) did not display more or larger atherosclerotic plaques than their ApoE(-/-) PGC-1α(+/+) littermates. In line with the previously published phenotype of PGC-1α(-/-) mice, ApoE(-/-) PGC-1α(-/-) mice had marked reduced body, liver and epididymal white adipose tissue (WAT) weight. VLDL/LDL-cholesterol and triglyceride contents were also reduced. Aortic expression of PPARα and PPARγ, two crucial regulators for adipocyte differentiation and glucose and lipid metabolism, as well as the expression of some PPAR target genes was significantly reduced in ApoE(-/-) PGC-1α(-/-) mice. Importantly, the epididymal WAT and aortic expression of IL-18 and IL-18 plasma levels, a pro-atherosclerotic cytokine, was markedly reduced in ApoE(-/-) PGC-1α(-/-) mice. CONCLUSIONS/SIGNIFICANCE: ApoE(-/-) PGC-1α(-/-) mice, similar as PGC-1α(-/-) mice exhibit markedly reduced total body and visceral fat weight. Since inflammation of visceral fat is a crucial trigger of atherogenesis, decreased visceral fat in PGC-1α-deficient mice may explain why these mice do not develop enhanced atherosclerosis.
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Registered trials
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