Calciprotein particles induce arterial stiffening ex vivo and impair vascular cell function.

ABSTRACT: Calciprotein particles (CPPs) are an endogenous buffering system, clearing excessive amounts of Ca²⁺ and PO₄^3- from the circulation and thereby preventing ectopic mineralization. CPPs circulate as primary CPPs (CPP1), which are small spherical colloidal particles, and can aggregate to form large, crystalline, secondary CPPs (CPP2). Even though it has been reported that CPPs are toxic to vascular smooth muscle cells (VSMC) in vitro, their effect(s) on the vasculature remain unclear. Here we have shown that CPP1, but not CPP2, increased arterial stiffness ex vivo. Interestingly, the effects were more pronounced in the abdominal infrarenal aorta compared to the thoracic descending aorta. Further, we demonstrated that CPP1 affected both endothelial and VSMC fun

SUBMITTER: Neutel CHG 

PROVIDER: S-EPMC11447031 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature