The role of p66Shc deletion in age-associated arterial dysfunction and disease states.
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Mitochondrial Oxidative Stress, Mitochondrial DNA Damage and Their Role in Age-Related Vascular DysfunctionAngiotensin II, NADPH oxidase, and redox signaling in the vasculatureRedox regulation of mitochondrial functionChronic matrix metalloproteinase inhibition retards age-associated arterial proinflammation and increase in blood pressureIdentification of Peroxiredoxin 1 as a novel interaction partner for the lifespan regulator protein p66Shc.CRIF1 deficiency induces p66shc-mediated oxidative stress and endothelial activation.European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS).Potential therapeutic benefits of strategies directed to mitochondria.Mechanisms of vascular aging: new perspectives.Dual role of endothelial nitric oxide synthase in oxidized LDL-induced, p66Shc-mediated oxidative stress in cultured human endothelial cells.Apurinic/apyrimidinic endonuclease 1 inhibits protein kinase C-mediated p66shc phosphorylation and vasoconstriction.Resistance exercise training increase activation of AKT-eNOS and Ref-1 expression by FOXO-1 activation in aorta of F344 ratsMicroparticles induce cell cycle arrest through redox-sensitive processes in endothelial cells: implications in vascular senescence.Habitual exercise and arterial aging.Recombinant adenovirus of human p66Shc inhibits MCF-7 cell proliferation.Role of mitochondrial dysfunction and altered autophagy in cardiovascular aging and disease: from mechanisms to therapeutics.Anti-aging medicine: molecular basis for endothelial cell-targeted strategies - a mini-review.Mitochondria and aging in the vascular system.p66Shc, a multifaceted protein linking Erk signalling, glucose metabolism, and oxidative stress.Endothelial nitric oxide synthase, vascular integrity and human exceptional longevity.Ageing, metabolism and cardiovascular disease.SIRT1 and SIRT6 Signaling Pathways in Cardiovascular Disease Protection.Central Role of Metabolism in Endothelial Cell Function and Vascular Disease.Arterial aging is risky.Prolonged swimming promotes cellular oxidative stress and p66Shc phosphorylation, but does not induce oxidative stress in mitochondria in the rat heart.Insights into the Shc Family of Adaptor Proteins.Deletion of the ageing gene p66(Shc) reduces early stroke size following ischaemia/reperfusion brain injury.Epigenetics and Immunometabolism in Diabetes and Aging.Immune enhancement effects and extraction optimization of polysaccharides from Citrus aurantium L. var. amara Engl.The expression of p66shc in peripheral blood monocytes is increased in patients with coronary heart disease and correlated with endothelium-dependent vasodilatation.Genetic deletion of the adaptor protein p66Shc increases susceptibility to short-term ischaemic myocardial injury via intracellular salvage pathways.
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The role of p66Shc deletion in age-associated arterial dysfunction and disease states.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 04 September 2008
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
The role of p66Shc deletion in age-associated arterial dysfunction and disease states.
@en
The role of p66Shc deletion in age-associated arterial dysfunction and disease states.
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type
label
The role of p66Shc deletion in age-associated arterial dysfunction and disease states.
@en
The role of p66Shc deletion in age-associated arterial dysfunction and disease states.
@nl
prefLabel
The role of p66Shc deletion in age-associated arterial dysfunction and disease states.
@en
The role of p66Shc deletion in age-associated arterial dysfunction and disease states.
@nl
P2860
P1476
The role of p66Shc deletion in age-associated arterial dysfunction and disease states
@en
P2093
Felix C Tanner
Thomas F Lüscher
P2860
P304
P356
10.1152/JAPPLPHYSIOL.90579.2008
P407
P577
2008-09-04T00:00:00Z