By Bradley S. Fleenor, Adam J. Berrones
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057232 References 39 38. Pierce GL, Zhu H, Darracott K, Edet I, Bhagatwala J, Huang Y, Dong Y (2013) Arterial stiffness and pulse-pressure amplification in overweight/obese African-American adolescents: relation with higher systolic and pulse pressure. Am J Hypertens 26(1):20–26. 1093/ ajh/hps014 39. Huynh Q, Blizzard L, Sharman J, Magnussen C, Schmidt M, Dwyer T, Venn A (2013) Relative contributions of adiposity in childhood and adulthood to vascular health of young adults. Atherosclerosis 228(1):259–264.
J Am Coll Cardiol 55(13):1318–1327. 061 13. Vlachopoulos C, Ioakeimidis N, Aznaouridis K, Terentes-Printzios D, Rokkas K, Aggelis A, Panagiotakos D, Stefanadis C (2014) Prediction of cardiovascular events with aortic stiffness in patients with erectile dysfunction. Hypertension 64(3):672–678. 03369 14. Vasan RS (2006) Biomarkers of cardiovascular disease: molecular basis and practical considerations. Circulation 113(19):2335–2362. 482570 15. Vigen R, Maddox TM, Allen LA (2012) Aging of the United States population: impact on heart failure.
Thus, examining the role of NFκB in arterial stiffness, and identifying novel interventions to modulate NFκB expression are promising [20, 34]. For example, inhibition of NFκB in older animals improves endothelium-dependent dilation via a NO-dependent mechanism. This finding indirectly suggests NFκB contributes to age-related aortic stiffness by reducing NO bioavailability and impairing endothelial function. As such, anti-inflammatory interventions may lead to reductions in aortic stiffness. Nitric Oxide (NO) Impaired endothelium-dependent dilation is a key functional outcome contributing to arterial stiffness.