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• W3160952226 abstract "The aorta and pulmonary arteries contain elastin, which confers elasticity to dampen the pulsatile force of cardiac systole. 1 O'Rourke M.F. Safar M.E. Dzau V. The cardiovascular continuum extended: aging effects on the aorta and microvasculature. Vasc Med. 2010; 15: 461-468 Crossref PubMed Scopus (136) Google Scholar Peripheral arteries are lined with smooth muscle cells, allowing for contraction and expansion to meet the needs of tissue blood flow. 2 Lacolley P. Regnault V. Laurent S. Mechanisms of arterial stiffening: from mechanotransduction to epigenetics. Arterioscler Thromb Vasc Biol. 2020; 40: 1055-1062 Crossref PubMed Scopus (13) Google Scholar Injury to either artery type leads to loss of pliability, resulting in damage to blood vessels and end organs. The two main factors leading to artery wall injury are as follows: (1) aging and (2) cardiometabolic disease risk factors. Aging per se leads to fracturing of extracellular elastin in the elastic arteries through repeated pulsatile stress. This process begins in a person’s fourth decade of life. 3 Wahart A. Hocine T. Albrecht C. et al. Role of elastin peptides and elastin receptor complex in metabolic and cardiovascular diseases. FEBS J. 2019; 286: 2980-2993 Crossref PubMed Scopus (20) Google Scholar In place of elastin, collagen is laid down and glycation of elastin remnants occurs. Elastin-derived remnants, in turn, reduce nitric oxide release from the endothelium and calcify the medial layer of the artery wall, further enhancing vessel wall stiffness. Regarding cardiometabolic disease, the insulin-resistant state is the core lesion appearing early in life, transitioning later in life to metabolic syndrome and prediabetes, and eventually to the end-stage manifestations of both metabolic (ie, type 2 diabetes [T2D]) and vascular disease (cardiovascular disease [CVD]). The insulin-resistant state is associated with vascular stiffness and endothelial dysfunction as a result of the accompanying inflammation, oxidative stress, dyslipidemia, advanced glycation end products, decreased generation of nitric oxide, activation of the renin-angiotensin system, and elevated blood pressure producing intimal medial wall injury, vascular smooth muscle proliferation, and atherothrombosis. 4 Galicia-Garcia U. Benito-Vicente A. Jebari S. et al. Pathophysiology of type 2 diabetes mellitus. Int J Mol Sci. 2020; 21: 6275 Crossref Scopus (32) Google Scholar" @default.
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• W3160952226 date "2021-06-01" @default.
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• W3160952226 title "Arterial Stiffness: Comment on the Article by Pavloska et al" @default.
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• W3160952226 doi "https://doi.org/10.1016/j.eprac.2021.04.002" @default.
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