Background The high cardiovascular morbidity and mortality of patients with CKD may result
in large part from medial vascular calcification, a process promoted by hyperphosphatemia
and involving osteo-/chondrogenic transdifferentiation of vascular smooth muscle cells
(VSMCs). Reduced serum zinc levels have frequently been observed in patients with CKD,
but the functional relevance of this remains unclear. Methods We performed experiments in
primary human aortic VSMCs; klotho-hypomorphic (kl/kl), subtotal nephrectomy, and …