Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 100, Issue 20, Pages 11201-11206Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1932554100
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Funding
- NCRR NIH HHS [K24RR017593-01, K24 RR017593] Funding Source: Medline
- NHLBI NIH HHS [R01 HL051980, HL51980, HL58555, HL51736, R29 HL051980, 7R01-HL43277-02] Funding Source: Medline
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Dystrc phic or ectopic mineral deposition occurs in many pathologic conditions, including atherosclerosis. Calcium mineral deposits that frequent y accompany atherosclerosis are readily quantifiable radiographically, serve as a surrogate marker for the disease, and predict a higher risk of myocardial infarction and death. Accelerating research interest has been propelled by a clear need to understand how plaquo structure, composition, and stability lead to devastating cardiovascular events. In atherosclerotic plaque, accumulating evidence is consistent with the notion that calcification involves the participation of arterial osteoblasts and osteoclasts. Here we summarize current models of intimal arterial plaque calcification and highlight intriguing questions that require further investigation. Because atherosclerosis is a chronic vascular inflammation, we propose that arterial plaque calcification is best conceptualized as a convergence of bone biology with vascular inflammatory pathobiology.
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