NDT Advance Access originally published online on March 7, 2006
Nephrology Dialysis Transplantation 2006 21(5):1166-1169; doi:10.1093/ndt/gfl089
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Editorial Comment
Vascular calcification—a matter of damage limitation?
Division of Cardiovascular Medicine, University of Cambridge, Box 110, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK
Correspondence and offprint requests to: Dr Catherine Shanahan, Department of Medicine, Division of Cardiovascular Medicine, ACCI, Level 6, Box 110, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK. Email: cs131@mole.bio.cam.ac.uk
Keywords: atherosclerosis; bone; calcification; Fetuin-A; matrix Gla protein; vascular smooth muscle cell; vesicles
| The first 150 words of the full text of this article appear below. |
 |
Introduction |
|---|
Vascular calcification has now been recognized as an important determinant of cardiovascular mortality in patients on dialysis. Recent cell biological studies, using phenotypically modulated, human vascular smooth muscle cells (VSMCs) in vitro, have highlighted the importance of vascular damage, leading to vesicle release, combined with loss of function of inhibitory proteins, as the major events in the calcification process. VSMC calcification is a regulated process, therefore the potential exists to inhibit progression or more significantly, induce regression. Identification of damage-inducing agents and calcification inhibitors is now quite advanced. The next challenge will be in determining ways to limit damage and induce expression and/or efficacy of inhibitors. Although new therapeutics have shown the potential to act on these pathways, there is still much to be learnt about how the complex ‘uraemic’ milieu appears to favour vascular calcification at the expense of bone mineralization.
Vascular calcification—two sites with different consequences
Vascular calcification or ‘hardening of the arteries’
Tissue mineralization and its regulating proteins
The cell biology of vascular calcification
Causes and consequences of vascular damage in dialysis
How to limit vascular damage in dialysis patients and help the inhibitors
What we do not know
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  C. Rinat, R. Becker-Cohen, A. Nir, S. Feinstein, D. Shemesh, N. Algur, E. Ben Shalom, B. Farber, and Y. Frishberg A comprehensive study of cardiovascular risk factors, cardiac function and vascular disease in children with chronic renal failure Nephrol. Dial. Transplant., November 23, 2009; (2009) gfp570v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. C. Shroff, R. McNair, N. Figg, J. N. Skepper, L. Schurgers, A. Gupta, M. Hiorns, A. E. Donald, J. Deanfield, L. Rees, et al. Dialysis Accelerates Medial Vascular Calcification in Part by Triggering Smooth Muscle Cell Apoptosis Circulation, October 21, 2008; 118(17): 1748 - 1757. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. R. Di Iorio, E. D'Avanzo, C. Piscopo, P. Grimaldi, E. Cucciniello, N. Cillo, and V. Bellizzi Progression of vascular calcification increases QT interval in haemodialysis patients Nephrol. Dial. Transplant., December 1, 2006; 21(12): 3609 - 3610. [Full Text] [PDF]
|
|