Calcification of arteries is a complex and dynamic process frequently seen in atherosclerosis, diabetes, and chronic kidney disease. This phenomenon, now considered a distinct inflammatory arteriopathy, has important clinical significance because arterial calcification is associated with increased cardiovascular events and is a strong predictor of poor cardiovascular outcomes.1,2 Patients with high coronary artery calcification scores have a five- to seven-fold increase in the risk of a hard coronary event compared with patients with low calcium scores, and patients with chronic kidney disease and vascular calcification have a 20- to 30-fold increase in cardiovascular mortality.2 Arterial calcification is a pathological process involving the vascular media and adventitia.3 Medial vascular smooth muscle cells (VSMCs) lose their ability to express smooth muscle-specific markers and undergo phenotypic transformation to osteoblast-like cells. Perivascular adventitial cells, microvascular pericytes, and adventitial mesenchymal stem cells also have the potential to express osteoblastic transcription factors, suggesting that, in addition to VSMCs, other vascular cell types contribute to calcification. The course of vascular calcification shares many features with that of bone mineralization, except that whereas skeletal mineralization is a physiological and highly regulated process, vascular calcification is a pathological phenomenon associated with extraskeletal mineralization in the vascular wall.2,3 Passive calcium phosphate deposition, active cell-mediated processes, and inflammatory responses contribute to vascular calcification.4 … *Corresponding author. Tel: +1 613 562 5800; fax: +1 613 562 5487. E-mail address : rtouyz{at}uottawa.ca
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