Association of Serum Phosphate and Related Factors in ESRD-Related Vascular Calcification
Figure 1
Mechanisms of VSMC osteogenesis during vascular calcification in chronic kidney disease. VSMC upregulate expression of transcription factors Osf2/Cbfa1 which were enhanced by ROS, leptin, vitamin D, increased CaxP product, or high PO4 (Pi) levels induced by Pit-1. VSMC activation occurs in part as a result of the phenotypic switch of VSMCs into osteoblast-like cells. VSMCs that have acquired an osteogenic phenotype express ALP and produce hydroxyapatite crystals. Calcification inhibitors such as PPi inhibit hydroxyapatite precipitation, whereas fetuin-A, MGP, OPG, OPN, and BMP-7 antagonize calcification. VSMC: Vascular smooth muscle cells, Osf2/Cbfa1: Osteoblast-specific transcription factor, ROS: Reactive oxygen species, CaxP product: Calciumx phosphate produce, PO4(Pi): Phosphate, Pit-1: Sodium-phosphate cotransporter-1, ALP: Alkaline phosphatase, PPi: Pyrophosphate, MGP: Matrix Gla protein, OPG: Osteoprotegerin, OPN: Osteopontin, BMP: Bone morphogenic protein.
