Regulation of vascular calcification in atherosclerosis.
Over a century ago it was recognized that the vessel wall is a predominant site for ectopic calcification which is a hallmark of clinically significant atherosclerotic lesions. Old observational studies, which characterized vascular calcification as osteogenesis, and recent identification of common molecular mechanisms in bone and vascular calcification have led to the new recognition that atherosclerotic calcification is an actively regulated process similar to osteogenesis and distinct from a metastatic passive mineralization. Since the atherosclerotic lesion is composed of a multitude of cells and inflammatory mediators, elucidation of the role of these components in induction and acceleration of calcification is of fundamental importance in better understanding its pathogenesis and identifying possible interventional targets. This article will focus on four important mediators of vascular calcification: 1) calcifying vascular cells, 2) oxidized lipids, 3) cytokines, and 4) leptin.
Parhami
F
F
Division of Cardiology, UCLA School of Medicine, Center for the Health Sciences, 47-123, 10833 Le Conte Avenue, Los Angeles, CA 90095, USA. fparhami@mednet.ucla.edu
Tintut
Y
Y
Patel
J K
JK
Mody
N
N
Hemmat
A
A
Demer
L L
LL
D001161:Arteriosclerosis / Q000473:pathology*; D002114:Calcinosis / Q000473:pathology*; D016207:Cytokines / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000473:pathology; D006801:Humans; D020738:Leptin / Q000378:metabolism*; D050356:Lipid Metabolism; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D009999:Ossification, Heterotopic / Q000473:pathology*
D016207:Cytokines; D020738:Leptin