Abstract
BACKGROUND: The bone-vascular axis plays a key role in the pathogenesis of vascular calcification (VC) in patients with chronic kidney disease (CKD). Understanding and managing the role of the bone-vascular axis in CKD-mineral and bone disorder (CKD-MBD) is critical for preventing and treating associated complications, including osteoporosis, arterial calcification, and cardiovascular diseases. This study aimed to comprehensively summarize the role of bone metabolism markers in uremic VC. SUMMARY: The skeleton, as an endocrine organ, can regulate systemic metabolic processes by secreting various bioactive substances. These molecules can induce the transdifferentiation of vascular smooth muscle cells, promoting their transition to other functional states, thereby affecting vascular growth and remodeling. KEY MESSAGES: The prevalence of VC in individuals with CKD is notably high. CKD-associated VC is characterized by the widespread accumulation of hydroxyapatite within the arterial media, which occurs as a result of the transformation of smooth muscle cells into osteoblastic smooth muscle cells under the influence of uremic toxins. Osteoblasts and osteoclasts in bone tissue secrete mineral metabolic proteins, which can influence neighboring cells, primarily vascular smooth muscle cells, through paracrine signaling. Both circulating and osteocytic sclerostin can exert a protective effect by inhibiting wingless/integrated (WNT)-induced calcification. The therapeutic goal for CKD-MBD is to reduce production of sclerostin by decreasing the osteogenic transdifferentiation of vascular smooth muscle cells. Calciprotein particles act as a physiological agent for delivering calcium-phosphate the bone and inducing fibroblast growth factor-23 expression in osteoblasts.