A novel role of cellular interactions in vascular calcification

Abstract

A series of clinical trials have confirmed the correlation between vascular calcification (VC) and cardiovascular events and mortality. However, current treatments have little effects on the regression of VC. Potent and illustrative mechanisms have been proven to exist in both bone metabolism and VC, indicating that these two processes share similarities in onset and progression. Multiple osteoblast-like cells and signaling pathways are involved in the process of VC. In this review, we summarized the roles of different osteoblast-like cells and we emphasized on how they communicated and interacted with each other using different signaling pathways. Further studies are needed to uncover the underlying mechanisms and to provide novel therapies for VC.

Keywords: Autophagy; Osteoblast-like cells; Signaling pathways; Vascular calcification.

Fig. 1

Schematic representation of osteoblast-like cells derived from different origins mediating VC. There are various origins of osteoblast-like cells in the vasculature, including ECs, pericytes, VSMCs, CVCs, myofibroblasts, and circulating progenitor cells. They collaboratively participate in the initiation and development of VC in the media or intima. CVCs calcifying vascular cells, ECs endothelial cells, MSC mesenchymal stem cell, VC vascular calcification, VSMCs vascular smooth muscle cells

Fig. 2

Overview of cellular interaction networks regulating calcification in the vascular wall (aortic intima, media, adventitia). During the formation of VC, there are constant cross-talks in the form exosomes among three layers of vascular wall. In addition, a complex of signaling network, including BMP, Wnt/β-catenin, AGEs and OPG/RANK/RANKL signaling pathways, are frequently seen in adventitia-media cross-talk or intima-media cross-talk. AGEs advanced glycation end products, BMP bone morphogenetic protein, OPG osteoprotegerin, RANK receptor activator of nuclear factor-kB, RANKL receptor activator of nuclear factor-kB ligand, VC vascular calcification