VSMCs are mainly composed of the medial layer of the blood vessels, which are subjected to mechanical stress and pressure of blood flow, and maintain vascular tone and resistance. Vascular smooth muscle cells are the predominant cell type in the arterial wall. Apoptosis in smooth muscle cells, oxidative stress, remodeling in extracellular matrix, and high levels of metalloproteinases increase vascular calcification, resulting in endothelial dysfunction. In addition, intracellular phosphate concentration increases in osteoblast-like cells due to developing hyperphosphatemia in chronic renal failure. Subsequently, the number of osteochondrogenic cells increases, and calcification inhibitors are suppressed an increased regulation of bone mineralization regulating genes and the release of calcified membrane-dependent carriers from smooth muscle cells in these calcifications are observed. Osteoblast-like cells that contain hydroxyapatite crystals appear in the extracellular matrix during vascular smooth muscle calcification. These cells may turn into osteoblasts and chondrocytes under stress. Vascular smooth muscle cells are of mesenchymal origin. Vascular smooth muscle cells (VSMCs) play an important role in the pathology of vascular calcifications. This effect is defined as the statin paradox. Despite the antilipidemic and anti-inflammatory effects of it, statins cause an increased calcification in vascular tissue with an unknown mechanism. Recently, it has been observed thanks to intravascular invasive images that the use of statins increases vascular calcification. The other causes of vascular calcification include smoking, male gender, and older age. Hypertension is associated with calcifications in the abdominal aorta.
Vascular calcifications associated with diabetes mellitus also affect the media and intima layer of vessels. Particularly severe aortic calcifications are seen in these patients. Another cause of vascular calcifications is familial hypercholesterolemia. Calcium deposits accumulate in vascular tissues as a result of secondary hyperparathyroidism that occurs in chronic renal failure. In addition to this, these calcifications may also occur as a complication of metabolic disorders in the end stage of chronic renal failure. Vascular calcifications often occur in the advanced stage of the atherosclerosis. There are several reasons leading to vascular calcifications ( Table 1). In this chapter, vascular calcification mechanism and its results will be discussed. The understanding of pathophysiology of cardiovascular diseases has an important role for the treatment success. Furthermore, they cause a significant burden on the health costs. As a result, increased vascular calcification is associated with cardiovascular mortality.Ĭardiovascular pathologies are still one of the most serious diseases in the world and are also known to be an important reason of mortality and morbidity. Increased arterial stiffness destroys vascular compliance, causes left ventricular hypertrophy, and disrupts coronary perfusion. Vascular and valvular calcifications are irreversible. Vascular calcification is due to arterial stiffness, stenosis, and occlusion. While the calcification seems in tunica intima layer of the vessel in atherosclerotic disease, it seems in tunica media layer of vessel in chronic renal failure with high uremic level. It is often observed calcification in cardiovascular system in some diseases such as chronic renal failure due to increased calcium-phosphate levels.
Phosphorus level is approximately 2.5–4.5 mg/dl in blood. Most of the phosphorus is present in the skeletal system. Phosphorus is more common than calcium in the human body. Parathormone and vitamin D regulate blood calcium levels. In total serum, the calcium level is approximately 8.8–10.4. Extracellular calcium levels are more than intracellular levels. It is has a crucial effect on intracellular and extracellular mechanisms. Calcium-phosphate levels have an effect on the vascular wall.
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