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BioMed Research International
Volume 2017 (2017), Article ID 7463590, 7 pages
Review Article

Calcifying Matrix Vesicles and Atherosclerosis

1Department of Molecular Genetic Diagnostics and Cell Biology, Division of Laboratory Medicine, Institute of Pediatrics, Research Center for Children’s Health, Moscow 119991, Russia
2Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Moscow 125315, Russia
3Unit of Atherosclerosis Prevention, Centro Cardiologico Monzino, IRCCS, 20138 Milan, Italy
4Federal Scientific Clinical Center for Resuscitation and Rehabilitation, 14-3 Solyanka Street, Moscow 109240, Russia
5Institute for Atherosclerosis Research, Skolkovo Innovative Center, Moscow 121609, Russia

Correspondence should be addressed to Veronika A. Myasoedova

Received 20 January 2017; Revised 3 March 2017; Accepted 11 October 2017; Published 7 November 2017

Academic Editor: Nishath Altaf

Copyright © 2017 Dimitry A. Chistiakov et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Artery calcification is a well-recognized predictor of late atherosclerotic complications. In the intima media, calcification starts with apoptosis of vascular smooth muscle cells (VSMCs) and the release of calcifying matrix vesicles with diameter of 0.5–15 μm that can be observed microscopically. In complicated plaques, calcification is generally less frequent. Calcifying vesicles are released by proatherosclerotic VSMCs into the collagen-rich matrix. The vesicles can penetrate into the intima media and protrude into the arterial lumen and thereby may represent a potential cause of atherothrombosis. In calcified fibrolipid plaques, the rate of calcification is increased but is followed with healing of a lesion rupture and exhibited by further erosion and/or intimal thickening. Generally, calcification directly correlates with the apoptosis of VSMCs and macrophages accompanied by the release of osteogenic matrix vesicles. This is a hallmark of atherosclerosis-related apoptosis of VSMCs that is commonly released in plaque stabilization.