Vascular calcification—a matter of damage limitation?

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Abstract
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.