ABSTRACT
BACKGROUND: Arterial calcification (AC) is a major health problem associated with extreme morbidity and a shortened survival. It is currently without any effective treatment. ATP and the purinergic system in general are now emerging as being important in the pathogenesis of AC and potentially provide a new focus for novel therapies. METHODS: This review systematically analyses and discusses the current literature examining the relevance of the purinergic system to AC. Particular emphasis is given to the enzymes associated with ATP metabolism and their role in maintaining a balance between promotion and inhibition of arterial mineralization. Points of controversy are highlighted, and areas for future research are suggested. CONCLUSION: The potential roles of ATP and the purinergic system in AC are beginning to be elucidated. While further work is necessary, current knowledge suggests that several components of the purinergic system could be targeted to develop new treatments for AC.
Subject(s)
Adenosine Triphosphate/physiology , Receptors, Purinergic/metabolism , Vascular Calcification/metabolism , Arteries , HumansABSTRACT
The discovery of fibroblast growth factor-23 (FGF-23) as a key regulator of phosphate and vitamin D metabolism has forced a rethink about the mineral and bone disorder of chronic kidney disease (CKD). FGF-23 powerfully predicts adverse cardiovascular outcomes in patients with CKD and an important question is whether treatment regimens should now be tailored to address FGF-23 levels in addition to those of calcium, phosphate, parathyroid hormone and vitamin D. Nevertheless, despite the known action of active vitamin D therapies to increase FGF-23, this should probably still form an important part of the management of patients with hyperparathyroidism and perhaps at low doses of essentially all patients with advanced renal disease.