Arterial aging: is it an immutable cardiovascular risk factor?
By S. Najjar, A. Scuteri, E. Lakatta. HYPERTENSION, 2005
677 citations recorded by the source corpus.
Subfields: Cardiology and Cardiovascular Medicine, Immunology
View Paper: https://www.semanticscholar.org/paper/9734fb9265b5a902b4c4a84463b04bfe40f6cfcd
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In Cardiology and Cardiovascular Medicine
In Immunology
Citations in the corpus
- Use of carotid ultrasound to identify subclinical vascular disease and evaluate cardiovascular disease risk: a consensus statement from the American Society of Echocardiography Carotid Intima-Media Thickness Task Force. Endorsed by the Society for Vascular Medicine. (2008, background): “It represents subclinical vascular disease, the pathophysiologic substrate that explains why CIMT is a risk factor and a marker of CVD risk.(56,57)”
- Renin‐angiotensin system revisited (2008, background): “Arterial components of the Ang II-signalling cascade increase with ageing [70] .”
- The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression (2010, background): “External mitogenic signals, for example growth-related oncogene alpha (GROα) secretion by tumor cells in close proximity to normal cells (32) or circulating angiotensin II (33, 34), have also been shown to induce cellular senescence.”
- An integrated view of oxidative stress in aging: basic mechanisms, functional effects, and pathological considerations. (2007, background): “While it is unclear whether longerterm antioxidant treatments might prove effective in dealing with aging and conditions, such as vascular aging, provocative results from acute-treatment studies suggest that the vasculature should be viewed as a key target for therapeutic intervention (133, 180, 239”
- Arterial stiffness, pressure and flow pulsatility and brain structure and function: the Age, Gene/Environment Susceptibility--Reykjavik study. (2011, background): “Increased CFPWV is associated with collagen deposition and fibrosis in the aortic wall (Najjar et al., 2005).”
- Senescent cells as a source of inflammatory factors for tumor progression (2010, background): “External mitogenic signals, for example growth-related oncogene alpha (GROα) secretion by tumor cells in close to normal cells [36] or circulating angiotensin II [37, 38], have also been shown to induce cellular senescence.”