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.
Keywords: Bone metabolism marker; Bone-vascular axis; Chronic kidney disease; Osteoporosis; Vascular calcification.
The bone-vascular axis is crucial in the pathogenesis of VC in CKD, impacting mineral and bone disorders and leading to complications like osteoporosis and cardiovascular diseases. This study focuses on the role of bone metabolism markers in uremic VC. The skeleton functions as an endocrine organ, releasing bioactive substances that facilitate the transdifferentiation of vascular smooth muscle cells (VSMCs) into osteoblastic cells, which contributes to vascular remodeling and calcification. Notably, circulating and osteocytic sclerostin can protect against calcification by inhibiting WNT signaling pathways. Therefore, a therapeutic goal for CKD-related mineral and bone disorder (CKD-MBD) is to lower sclerostin levels to reduce VSMC transdifferentiation. Additionally, calciprotein particles play a role in regulating calcium-phosphate transport to bones and stimulating fibroblast growth factor-23 expression in osteoblasts. Understanding these mechanisms is essential for developing effective strategies to manage VC in CKD patients.
© 2024 The Author(s). Published by S. Karger AG, Basel.