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• W2912352298 abstract "Itai-itai disease is an endemic disease characterized by osteomalacia accompanied with osteoporosis and multiple proximal tubular dysfunctions (Fanconi syndrome). Itai-itai disease is caused by environmental cadmium exposure, but the pathological mechanism of the disease remains unknown. Cadmium also yields irreversible bone and renal dysfunction; new validated biomarkers are needed for the detection of cadmium-induced nephropathy. We have focused on the role of fibroblast growth factor (FGF) 23, a protein that is essential for phosphate homeostasis in the bone-kidney axis, and have investigated the mechanism of cadmium-induced FGF23 production by bone cells. Cadmium injection in mice resulted in increased plasma FGF23 concentrations, but the level of FGF23 mRNA in the bone was not changed. Further studies indicated that increased plasma FGF23 levels in the cadmium-injected mice were caused by the posttranslational regulation of the FGF23 protein stability. FGF23 stability and secretion was altered by glycosylation of FGF23, which was in turn regulated by the activity of the GalNAc-T3 protein. We demonstrated that expression of the GalNAc-T3-encoding gene was significantly increased by cadmium exposure. Moreover, cadmium-dependent FGF23 accumulation was inhibited by an antagonist of the aryl hydrocarbon receptor (AhR), a transcription factor that can bind to the promoter of the GalNAc-T3 gene. Thus, cadmium stimulates transcription of the GalNAc-T3 gene via enhanced binding of AhR to the GalNAc-T3 promoter." @default.
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• W2912352298 date "2019-01-01" @default.
• W2912352298 modified "2023-10-18" @default.
• W2912352298 title "Disturbance in Phosphorus Metabolism by Cadmium Exposure" @default.
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• W2912352298 doi "https://doi.org/10.1007/978-981-13-3630-0_14" @default.
• W2912352298 hasPublicationYear "2019" @default.
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