血管異位性鈣化的機制(1)：成骨作用的引發

Mechanism of Vascular Ectopic Calcification (1)-Induction of Osteogenesis

陳鴻毅 ； 楊芝青

《中華民國血液淨化醫學會雜誌》 12卷3期 (2007/09) Pp. 35-44

https://doi.org/10.30024/JFBPS.200709.0003

並列摘要

Ectopic calcification has been noted in the vasculature for many decades. Vascular calcification is a consequence of tightly regulated processes with competition between factors promoting calcification and inhibitors of mineralization, but the precise mechanisms facilitating ectopic mineral deposition are unclear. One major hypothesis of vascular calcification is that it is a consequence of active bone formation in situ by osteoblast-type cells. These cells may be derived from stem cells (circulating or within the vessel wall) or differentiation of existing cells, such as smooth muscle cells (SMCs) or pericytes. Once the osteogenic phenotype is induced, cells gain a distinctive molecular fingerprint, marked by the transcription factor core binding factor-α1.
The ability to undergo reversible differentiation is characteristic of the VSMC phenotype; these cells are in their differentiated, contractile form at baseline but respond to various stimuli then entering into a proliferative, synthetic state to produce extracellular matrix (ECM). Several stimuli induce VSMCs to undergo osteogenic differentiation, including oxidative stress, bone morphogenetic proteins (BMPs), or changes in pyrophosphate levels etc. Additionally, there is several evidence that implicate neoangiogenesis as a necessary requirement for vascular and valvular calcification. Neovascularization is abundant in areas of lesional calcification.
The mechanism of the colocalization of angiogenesis and calcification is likely multifactorial as these processes involve the coordinated interplay of vascular endothelial and SMCs, pericytes, circulating and resident osteoprogenitors, as well as osteoblastic cells. Cytokines, such as BMP-2 and BMP-4, and the angiogenic factor vascular endothelial growth factor (VEGF) stimulate migration and differentiation of osteoblasts. VEGF was elaborated by osteoblasts and chondrocytes and VEGF receptors were localized on these cell types as well as chondrocytes. VEGF modulates the function and phenotype of these cells and stimulates chondrocytes activity. Newly formed vessels may simply serve as a conduit to deliver stem and other progenitor cells to new areas of the lesion.

並列關鍵字

ectopic calcification ； neoangiogenesis ； osteogenic differentiation ； smooth muscle cells