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Updated: Jun 30, 2026

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
[Extracellular matrix, matrix-degrading proteases and vascular calcification]
Yao-Yao Du1, Xian Wang, Wei Kong
1Department of Physiology and Pathophysiology, Peking University Health Science Center, Beijing 100083, China.
Abstract:
Vascular calcification is a common phenomena among atherosclerosis, diabetes, chronic kidney failure and aging. Recently, extensive researches have shown that the mechanisms of vascular calcification share great similarity with physiological mineralization rather than a passive deposition of calcium and phosphate. As a major component of blood vessels, the extracellular matrix (ECM) proteins not only provide a scaffold for normal vasculature, but also regulate the attachment, proliferation, migration and differentiation of vascular cells through ECM-cell interaction. Furthermore, it also serves as a reservoir for growth factors or cytokines. Previous studies have indicated the potential importance of ECM and ECM degrading proteases during vascular calcification. Extracellular matrix not only provides a major site for calcium and phosphate deposition, but also actively participates in the process of calcification through an accelerating or inhibitory effect. Multiple extracellular matrix proteins have been altered during the calcification. The disturbance of the delicate balance of ECM homeostasis may affect the evolution of vascular calcification. On the other hand, matrix degrading proteases (such as MMPs) may be involved in the occurrence and development of vascular calcification by affecting matrix or non-matrix substances (such as cytokines or growth factors). The current review summarizes the recent advance on vascular calcification in the context of ECM and MMPs.
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