Vascular Calcification, Insight in Its Pathophysiological Pathways, Genetics and Clinical Aspects

Abstract

The pathophysiology and genetic regulation of this process are both evaluated in this chapter along with the key mechanisms at play. Vascular calcification is highly associated with cardiovascular disease mortality, particularly in high risk patients with diabetes and chronic kidney diseases (CKD). In blood vessels, intimal calcification is associated with atherosclerosis, whereas medial calcification is a non-occlusive process which leads to increased vascular stiffness and reduced vascular compliance. In the valves, calcification of the leaflets can change the mechanical properties of the tissue and result in stenosis. For many decades, vascular calcification has been noted as a consequence of aging. Recent research suggests that arterial calcification is an independent cardiovascular risk factor (CRF) for morbidity and mortality. New studies have pointed out the existence of complex physiopathological mechanisms that flocks inflammation, oxidation, the release of chemical mediators, and genetic factors that promote the osteochondrogenic differentiation of vascular smooth muscle cells (VSMC).