Dear Colleagues,
Aging impairs blood vessel function and leads to cardiovascular disease. Characteristic features of large and small arteries that occur with aging include endothelial dysfunction, vascular remodeling, inflammation, vascular calcification, and increased arterial stiffness. Arterial changes may impact the severity of vascular damage in patients with hypertension, diabetes mellitus, hyperlipidemia, and the metabolic syndrome. Vascular calcification is characterized by mineral deposition in the form of calcium-phosphate complexes and is thought to play an important role in the normal aging process. Vascular calcification is the major cause of arterial stiffness in patients with chronic kidney disease (CKD). Arterial stiffness decreases nitric oxide (NO) production, resulting in vascular smooth muscle cells (VSMCs) being similar to bone formation (osteochondrogenic differentiation) and endothelial cells into mesenchymal cells (endothelial to mesenchymal transition). The imbalance between calcification inhibitors and inducers is considered a key feature in the pathology of vascular calcification. The mechanisms associated with vascular calcification include inflammation, the production of reactive oxygen species (ROS), apoptosis, matrix vesicle release, remodeling of the extracellular matrix and elastin degradation. The aim of this Special Issue is to offer a platform, both for clinicians and basic researchers, to present and discuss novel issues in the pathophysiology of vascular calcification in cardiovascular disease. We anticipate that these pubications will significantly contribute to a better understanding of vascular calcification in cardiovascular disease and will address both traditional and non-traditional risk factors that are essential to reducing the risk of vascular calcification in patients with cardiovascular disease.
Prof. Bang-Gee Hsu
Guest Editor
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