Abstract
Arterial calcification refers to the abnormal deposition of calcium salts in the arterial wall, which results in vessel lumen stenosis and vascular remodeling. Studies increasingly show that arterial calcification is a cell mediated, reversible and active regulated process similar to physiological bone mineralization. The osteoblasts and chondrocytes-like cells are present in large numbers in the calcified lesions, and express osteogenic transcription factor and bone matrix proteins that are known to initiate and promote arterial calcification. In addition, osteoclast-like cells have also been detected in calcified arterial walls wherein they possibly inhibit vascular calcification, similar to the catabolic process of bone mineral resorption. Therefore, tilting the balance between osteoblast-like and osteoclast-like cells to the latter maybe a promising therapeutic strategy against vascular calcification. In this review, we have summarized the current findings on the origin and functions of osteoblast-like and osteoclast-like cells in the development and progression of vascular progression, and explored novel therapeutic possibilities.
Highlights
Vascular calcification, or the pathological accumulation of calcium phosphate crystals in the intimal and medial layers of vessel walls, is the pathological basis of many cardiovascular diseases [1, 2]
The research of Malhotra et al shows endothelial-mesenchymal transition (EndMT) and vascular calcification in vitro and in vivo are dependent upon bone morphogenetic protein (BMP) signaling in matrix gla protein (MGP)-deficient mice, while the other hand, suggests that activation of BMP signaling inhibits atherosclerosis in MGP-deficient mice fed a standard diet when compared to LDLR–/– mice fed a high fat diet, a murine model of atherosclerosis [73]. These results indicate that vascular endothelial cells (VECs) can transdifferentiate into osteoblast-like cells and promote vascular calcification
Consistent with the above, pericytes cultured with high content of advanced glycation end products, beta- glycerophosphate or glucocorticoid differentiate into osteoblast-like cells expressing Runx2, alkaline phosphatase (ALP), OC and other bone-related genes, and form calcium nodules
Summary
The pathological accumulation of calcium phosphate crystals in the intimal and medial layers of vessel walls, is the pathological basis of many cardiovascular diseases [1, 2]. Consistent with the above, pericytes cultured with high content of advanced glycation end products, beta- glycerophosphate or glucocorticoid differentiate into osteoblast-like cells expressing Runx, ALP, OC and other bone-related genes, and form calcium nodules The latter may block MGP, an inhibitor of BMP4 and OPN, and activate the Axl signaling pathway [82,83,84]. Lin et al reported SMC-specific Runx knockout significantly reduced vascular osteochondrogenesis and calcification in mouse [10] These results suggest it is possible to treat vascular calcification at cellular level by regulating phenotype changes of VSMCs. In addition, owing mineral resorption capacity of osteoclast-like cells, osteoclasts efficiently remove deposited minerals from calcified elastin both in vitro and in vivo [40]. Cell treatment for vascular calcification based on osteoclast-like cells or macrophages and even MSCs is possible, but there are still some controversies and more research is needed
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
