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Year : 2017  |  Volume : 4  |  Issue : 1  |  Page : 3-14

Molecular mediators and controlling mechanism of vascular calcification

1 Department of Biomedical Sciences, College of Health Sciences, Arsi University, Asela, Ethiopia
2 Department of Biomedical Sciences, College of Public Health and Medical Sciences, Jimma University, Jimma, Ethiopia

Correspondence Address:
Leta Melaku
Department of Biomedical Sciences, College of Health Sciences, Arsi University, Asela
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijcep.ijcep_3_17

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Bone formation involves hydroxyapatite crystals, whose development begins in matrix vesicles that bud from osteoblasts. Vascular smooth muscle cells that have undergone osteoblast differentiation are also able to release similar vesicles with shared protein content. Such differentiation is restrained or inhibited under normal conditions, and there is a balance with osteoclast differentiation experienced by monocytes and macrophages within the vascular wall. Moreover, the reaction which allows crystal growth is thermodynamically unfavorable and is inhibited by pyrophosphate. In some situations, physiological balance is broken and vascular calcification (VC) is able to progress. VC has traditionally been considered to be a passive process that was associated with advanced age, atherosclerosis, uncommon genetic diseases, and some metabolic alterations such as diabetes mellitus and end-stage kidney failure. However, in the last years, VC has been proven to be an active and regulated process, similar to bone mineralization, in which different bone-related proteins are involved. VCs are actively regulated biological processes associated with crystallization of hydroxyapatite in the extracellular matrix and in cells of the media or intima of the arterial wall. Both patterns of VC often coincide and occur in patients with type II diabetes, chronic kidney disease, and other less frequent disorders; VCs are also typical in senile degeneration. Recent results question the classic classification of VC into intimal and medial calcification, at least in capacitance arteries. Pro- and anti-calcifying mechanisms play an active role in calcium deposit ion in vascular cells, making this area an active focus of research.

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