It is commonly accepted that the first cause of morbidity and mortality in chronic kidney disease (CKD) is the cardiovascular (CV) disease, in which vascular calcification (VC) plays a central pathogenetic role. In CKD population, mineral metabolism disorders have been recently investigated not only as key factors on renal osteodystrophy but also as inducing players on extra-skeletal calcification. Clearly, either high phosphate (P) or high calcium (Ca) concentration induce vascular smooth muscle cells mineralization in vitro studies. In fact, VC is induced by a cell-mediated process, which actively accompanies the traditional and passive Ca-P deposition in arterial walls. Interestingly, lack of inhibitory proteins, such as fetuin-A (alpha2-HS glycoprotein, AHSG), matrix GLA protein (MGP), osteoprotegerin (OPG), and bone morphogenetic protein 7 (BMP-7) are the regulatory key factors in preventing VC in uremic conditions.

The bone-vasculature-axis interaction: new insights into the pathogenesis of vascular calcification / M. Cozzolino, A. Galassi, A. Bellasi, M. Gallieni, D. Brancaccio. - In: GIORNALE ITALIANO DI NEFROLOGIA. - ISSN 0393-5590. - 24:5(2007 Sep), pp. 409-414.

The bone-vasculature-axis interaction: new insights into the pathogenesis of vascular calcification

M. Cozzolino;A. Bellasi;M. Gallieni;D. Brancaccio
2007-09

Abstract

It is commonly accepted that the first cause of morbidity and mortality in chronic kidney disease (CKD) is the cardiovascular (CV) disease, in which vascular calcification (VC) plays a central pathogenetic role. In CKD population, mineral metabolism disorders have been recently investigated not only as key factors on renal osteodystrophy but also as inducing players on extra-skeletal calcification. Clearly, either high phosphate (P) or high calcium (Ca) concentration induce vascular smooth muscle cells mineralization in vitro studies. In fact, VC is induced by a cell-mediated process, which actively accompanies the traditional and passive Ca-P deposition in arterial walls. Interestingly, lack of inhibitory proteins, such as fetuin-A (alpha2-HS glycoprotein, AHSG), matrix GLA protein (MGP), osteoprotegerin (OPG), and bone morphogenetic protein 7 (BMP-7) are the regulatory key factors in preventing VC in uremic conditions.
Settore MED/14 - Nefrologia
GIORNALE ITALIANO DI NEFROLOGIA
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2434/43400
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