Vascular calcification and its relation to bone calcification: Possible underlying mechanisms

被引:45
作者
Mody, N
Tintut, Y
Radcliff, K
Demer, LL
机构
[1] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90024 USA
[2] Univ Calif Los Angeles, David Geffen Sch Med, Dept Physiol, Los Angeles, CA 90024 USA
关键词
D O I
10.1067/mnc.2003.0012
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Significant scientific and clinical advances have been achieved in the study of vascular calcification during the last 10 years. Vascular calcification occurs frequently in atheromas and carries significant risk for future cardiac events due to stenotic and hemodynamic effects. The constituents of bone matrix and mineralization are present in atherosclerotic lesions, and a population of cells that secrete these products in vitro has been identified. The phenotype of these cells and their capacity to secrete osteoid are under the control of numerous inflammatory mediators and are thought to be regulated by similar molecular mechanisms as osteogenesis. Clinically, further studies are required to precisely define the prevalence of vascular calcification and its correlation with atherosclerotic disease, including risk factors for atherothrombotic disease such as smoking, diabetes, dyslipidemia, and sedentary lifestyle. Many other issues remain to be addressed including the following: the origin of subpopulations of progenitor cells within the arterial tree, other differentiation capacity of these progenitor cells, factors that control their migration, and the presence of a common molecular regulatory motif of bone development linking atherogenesis and osteoporosis.
引用
收藏
页码:177 / 183
页数:7
相关论文
共 52 条
[1]  
AUBIN JE, 1993, CELLULAR MOL BIOL BO, P2
[2]   Relationship of clinical presentation and calcification of culprit coronary artery stenoses [J].
Beckman, JA ;
Ganz, J ;
Creager, MA ;
Ganz, P ;
Kinlay, S .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2001, 21 (10) :1618-1622
[3]   INITIATION AND PROGRESSION OF MINERALIZATION OF BONE NODULES FORMED INVITRO - THE ROLE OF ALKALINE-PHOSPHATASE AND ORGANIC PHOSPHATE [J].
BELLOWS, CG ;
AUBIN, JE ;
HEERSCHE, JNM .
BONE AND MINERAL, 1991, 14 (01) :27-40
[4]   BONE MORPHOGENETIC PROTEIN EXPRESSION IN HUMAN ATHEROSCLEROTIC LESIONS [J].
BOSTROM, K ;
WATSON, KE ;
HORN, S ;
WORTHAM, C ;
HERMAN, IM ;
DEMER, LL .
JOURNAL OF CLINICAL INVESTIGATION, 1993, 91 (04) :1800-1809
[5]   Matrix GLA protein modulates differentiation induced by done morphogenetic protein-2 in C3H10T1/2 cells [J].
Bostrom, K ;
Tsao, D ;
Shen, S ;
Wang, Y ;
Demer, LL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (17) :14044-14052
[6]  
Boström K, 2000, CRIT REV EUKAR GENE, V10, P151
[7]   osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification [J].
Bucay, N ;
Sarosi, I ;
Dunstan, CR ;
Morony, S ;
Tarpley, J ;
Capparelli, C ;
Scully, S ;
Tan, HL ;
Xu, WL ;
Lacey, DL ;
Boyle, WJ ;
Simonet, WS .
GENES & DEVELOPMENT, 1998, 12 (09) :1260-1268
[8]   Increased bone formation in osteocalcin-deficient mice [J].
Ducy, P ;
Desbois, C ;
Boyce, B ;
Pinero, G ;
Story, B ;
Dunstan, C ;
Smith, E ;
Bonadio, J ;
Goldstein, S ;
Gundberg, C ;
Bradley, A ;
Karsenty, G .
NATURE, 1996, 382 (6590) :448-452
[9]   Osf2/Cbfa1: A transcriptional activator of osteoblast differentiation [J].
Ducy, P ;
Zhang, R ;
Geoffroy, V ;
Ridall, AL ;
Karsenty, G .
CELL, 1997, 89 (05) :747-754
[10]  
FAVUS MJ, 1999, PRIMER METABOLIC BON, P3