Role of calcification in aortic degeneration

Abstract

Vascular calcification is a widely-spread pathology with high mortality. It is active bioregulated process that is observed in pathogenesis of different desires, associated with metabolic dysfunction, congenital tissue desires and aging. Signal pathways and transcription factors that are involved in vascular calcification are also takes place in normal osteogenesis and/or vascular development. In the review the main attention is payed to the role of signaling pathways BMP (bone morphogenic protein), Notch, Wnt and to the role of transcription factors BMP2, RUNX2, Msx2 in vascular calcification. Probably, dysfunction of osteogenic signal pathways and transdifferentiation of vascular cells to osteoblast-like cells is a common prosses not only for vascular calcification or mineralization, but is a way of vascular degradation in general. Proosteogenic changes at cellular and molecular level may play role in pathogenesis of a disease without manifestation of vascular mineralization, such as thoracic aortic aneurysm. Ability of vascular cells to change their phenotype to osteophenotype is very likely biologically important ability. Over weakness of calcific signaling pathways activity can also lead to vascular pathology. The aim of the review is to overlook the mechanisms of vascular calcification focusing at the role of signal pathways and vascular cells at this process with particular attention to aortic calcification. Understanding the mechanisms of biological regulation of pro- and antiosteogenic processes in pathology and normal conditions opens new opportunities to influence this prosess in order to correct vascular pathologies.