ArticleJournal of biomedical science2009
Enhanced susceptibility of cyclin kinase inhibitor p21 knockout mice to high fat diet induced atherosclerosis.
Article in Journal of biomedical science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- The role of cellular senescence in cardiovascular disease.Cell death discovery · 2025Review
- Unveiling the role of ABI3 and hub senescence-related genes in macrophage senescence for atherosclerotic plaque progression.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Association between atherogenic risk-modulating proteins and endothelium-dependent flow-mediated dilation in coronary artery disease patients.European journal of applied physiology · 2023Article
- DNA damage response signaling: A common link between cancer and cardiovascular diseases.Cancer medicine · 2023Review
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- Time-dependent replicative senescence vs. disturbed flow-induced pre-mature aging in atherosclerosis.Redox biology · 2020Review
- The Role of Protein SUMOylation in the Pathogenesis of Atherosclerosis.Journal of clinical medicine · 2019Review
- Senescent cells in the development of cardiometabolic disease.Current opinion in lipidology · 2019Review
- High-fat diets promote colon orthotopic transplantation tumor metastasis in BALB/c mice.Oncology letters · 2019Article
- Senescent cells: a therapeutic target for cardiovascular disease.The Journal of clinical investigation · 2018Review
- MicroRNA-296: a promising target in the pathogenesis of atherosclerosis?Molecular medicine (Cambridge, Mass.) · 2018Review
- Senescent cells: an emerging target for diseases of ageing.Nature reviews. Drug discovery · 2017Review
- Senescent intimal foam cells are deleterious at all stages of atherosclerosis.Science (New York, N.Y.) · 2016Article
- Cellular senescence in aging and age-related disease: from mechanisms to therapy.Nature medicine · 2015Review
- Review
- The COP9 signalosome and vascular function: intriguing possibilities?American journal of cardiovascular disease · 2015Review
- The emerging role of senescent cells in tissue homeostasis and pathophysiology.Pathobiology of aging & age related diseases · 2015Article
- SIRT1-mediated epigenetic downregulation of plasminogen activator inhibitor-1 prevents vascular endothelial replicative senescence.Aging cell · 2014Article
- Cellular senescence: from physiology to pathology.Nature reviews. Molecular cell biology · 2014Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclin kinase inhibitor p21 is one of the most potent inhibitors of aortic smooth muscle cell proliferation, a key mediator of atherosclerosis. This study tests if p2l deficiency will result in severe atherosclerosis in a mouse model. p21-/- and strain matched wild type mice were fed with high fat diet for 21 weeks. Analysis for biochemical parameters (cholesterol, triglycerides) in serum and mRNA expression of CD36, HO-1, TGF-beta, IFN-gamma, TNF-alpha, PPAR-gamma and NADPH oxidase components (p22phox, NOX-1 and Rac-1) was performed in aortic tissues by Real Time PCR. p21-/- mice gained significantly (p < 0.01) more weight than wild type mice, triglycerides (p < 0.05) and cholesterol levels (p < 0.01) were more pronounced in the sera of p21-/- compared to wild type mice fed with high fat diet. High fat diet resulted in significantly decreased TGF-beta (p < 0.02), HO-l (p < 0.02) and increased CD36 (p < 0.03) mRNA expression in aortic tissues of p21-/- mice compared to animal fed with regular diet. IFN-gamma mRNA expression (235 +/- 11 folds) increased significantly in high fat diet fed p21-/- mice and a multifold modulation of PPAR-gamma(136 +/- 7), p22phox, NOX-1 and Rac-1 (15-35-folds) mRNA in aortic tissues from p21-/- mice compared to the wild type mice. Severity of atherosclerotic lesions was significantly higher in p21-/- compared to wild type mice. The results demonstrate that the deficiency of p21 leads to altered expression of pro-atherogenic genes, and severe atherosclerosis in mice fed with high fat diet. This opens the possibility of p21 protein as a therapeutic tool to control progression of atherosclerosis.
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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.