Albiero Mattia, Avogaro Angelo, Fadini Gian Paolo
Department of Medicine, University Hospital of Padova, Via Giustiniani, 2, 35100 Padova, Italy.
Curr Pharm Des. 2014;20(37):5889-96. doi: 10.2174/1381612820666140212193848.
Vascular calcification is the deposition of calcium-phosphate salts in the form of hydroxyapatite within the arterial wall. This is a finely regulated process to such an extent that it shares some mechanisms with endochondral and membranous embryonic ossification. Current theories describe vascular calcification as the imbalance between mechanisms, which promote calcification and those that inhibit it. Canonical cellular players in this scenario include endothelial cells, resident vascular smooth muscle cells and immune cells. Nevertheless, the last decade has seen the rise of extraparietal cells as important players in vascular biology and also in the setting of ectopic calcification. After an overview of the mechanism involved in vascular calcification, we herein discuss the potential role of different populations of circulating calcifying cells.
血管钙化是磷酸钙盐以羟基磷灰石的形式在动脉壁内沉积。这是一个精细调控的过程，在某种程度上它与软骨内和膜性胚胎骨化有一些共同机制。当前理论将血管钙化描述为促进钙化和抑制钙化的机制之间的失衡。在这种情况下，典型的细胞参与者包括内皮细胞、血管平滑肌驻留细胞和免疫细胞。然而，在过去十年中，壁外细胞已成为血管生物学以及异位钙化过程中的重要参与者。在概述了血管钙化所涉及的机制之后，我们在此讨论不同群体循环钙化细胞的潜在作用。
