Nephrol Dial Transplant (2000) 15: 1272-1274
© 2000 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
Vascular calcification—a passive process in need of inhibitors
Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA
Keywords: arteries; calcification; matrix GLA protein; osteoprotegerin; extracellular matrix
Introduction
Vascular calcification occurs frequently in atherosclerotic lesions. In addition, several inherited diseases have been described that are characterized by isolated medial calcification of arteries. The existence of such diseases, together with some recently developed mouse models, indicates that vascular calcification and atherosclerosis are different genetic entities that can be studied separately. Our understanding of the genetic basis of vascular calcification has significantly increased after mouse genetics became available. The generation of two mutant mouse strains, i.e. mice lacking matrix GLA protein or osteoprotegerin, has had the biggest impact on vascular calcification as both strains display isolated medial calcification of arteries. These phenotypes demonstrate that vascular calcification is mostly a passive process and that its inhibition is genetically controlled.
Calcification of atherosclerotic lesions
Atherosclerosis is the major cause of mortality in the Western hemisphere [1]. It is characterized by the presence of atherosclerotic lesions in the arterial intima leading to narrowing of the
Vascular calcification in the absence of atherosclerosis
Matrix GLA protein and osteoprotegerin are required to prevent calcification of mouse arteries
Inhibition of mineralization is genetically controlled
Concluding remarks
Notes
References
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