Towards a better understanding of arterial calcification disease progression in CKD: investigation of early pathological alterations.

Background: Cardiovascular disease remains the leading cause of death in chronic kidney disease (CKD) patients, especially in those undergoing dialysis and kidney transplant surgery. CKD patients are at high risk of developing arterial media calcifications (AMC) and arterial stiffness. We hypothesized that investigation of disease progression at an early stage could provide novel insights in understanding AMC etiology.

Endothelial dysfunction aggravates arterial media calcification in warfarin administered rats.

Arterial media calcification is an active cell process. This encompasses osteochondrogenic transdifferentiation of vascular smooth muscle cells followed by the deposition of calcium-phosphate crystals. Increasing evidence suggests a significant role for endothelial cells (ECs) in the development of arterial media calcification.

Endothelial Contribution to Warfarin-Induced Arterial Media Calcification in Mice.

Arterial media calcification (AMC) is predominantly regulated by vascular smooth muscle cells (VSMCs), which transdifferentiate into pro-calcifying cells. In contrast, there is little evidence for endothelial cells playing a role in the disease. The current study investigates cellular functioning and molecular pathways underlying AMC, respectively by, an ex vivo isometric organ bath set-up to explore the interaction between VSMCs and ECs and quantitative proteomics followed by functional pathway interpretation.

The Vicious Cycle of Arterial Stiffness and Arterial Media Calcification.

Arterial media calcification and arterial stiffness are independent predictors of cardiovascular mortality. Both processes reinforce one another, creating a vicious cycle in which transdifferentiation of endothelial cells and vascular smooth muscle cells play a central role. Physiological functioning of vascular smooth muscle cells in the arterial medial layer greatly depends on normal endothelial cell behavior.