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Critical Reviews™ in Eukaryotic Gene Expression
Fator do impacto: 1.841 FI de cinco anos: 1.927 SJR: 0.627 SNIP: 0.516 CiteScore™: 1.96

ISSN Imprimir: 1045-4403
ISSN On-line: 2162-6502

Critical Reviews™ in Eukaryotic Gene Expression

DOI: 10.1615/CritRevEukarGeneExpr.v10.i2.40
8 pages

Regulatory Mechanisms in Vascular Calcification

Kristina Bostrom
Division of Cardiology, Departments of Medicine and Physiology, UCLA School of Medicine, Los Angeles, CA 90095-1679
Linda L. Demer
Division of Cardiology, Departments of Medicine and Physiology, UCLA School of Medicine, Los Angeles, CA 90095-1679

RESUMO

Vascular calcification is increasingly recognized as a significant contributor to cardiovascular morbidity and mortality as well as a biologically regulated process potentially subject to prevention and reversal.
Both coronary and aortic calcification are common and influence plaque rupture, angioplasty and surgical complications, and compensatory enlargement. Aortic calcification increases aortic rigidity and contributes to cadiac ischemia, left ventricular hypertrophy, heart failure, and stroke. Calcification is also common in aortic valve leaflets further compounding adverse hemodynamic effects.
Vascular calcification has often been attributed to "passive" crystallization. However, functional similarities between atherosclerotic lesions and bone contradict this view and indicate that it is no more "passive" than in embryonic bone formation or bone repair. Similarities include presence of all the major components of bone osteoid, bone regulatory factors, and subpopulations of artery wall cells that retain osteoblastic lineage potential.
Several animal models for vascular calcification are available. Spontaneous vascular calcification occurs in null mice for matrix GLA protein (MGP), a small matrix protein of unknown function, and osteoprotegerin (OPG), known to modulate osteoclast differentiation. Vascular calcification may also be induced by feeding vitamin D and calcium or warfarin to normal animals, or by fat-feeding mice null for apoE or the LDL-receptor.
Overall, regulation of vascular calcification is a growing field with surprising mechanisms and connections to other fields of biology.


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