Abstract
Background and Aims : Calciprotein particles (CPPs), generated in human blood to cope with mineral stress, mediate aggregation and clearance of excessive calcium and phosphate from the circulation. However, increased serum propensity to produce CPPs has been associated with arterial hypertension, cerebrovascular disease, myocardial infarction, and cardiovascular death by causing endothelial dysfunction. As CPPs might represent a link between disturbed mineral homeostasis and cardiovascular disease, we conducted ex vivo testing of potential anti-CPP treatment modalities: albumin (Ca2+-binding protein), Mg2+ supplementation and chelation therapy.
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