First published February 2, 2009 - More info
Given the dramatic increase in skeletal size during growth, the need to preserve skeletal mass during adulthood, and the large capacity of bone to store calcium and phosphate, juxtaposed with the essential role of phosphate in energy metabolism and the adverse effects of hyperphosphatemia, it is not surprising that a complex systems biology has evolved that permits cross-talk between bone and other organs to adjust phosphate balance and bone mineralization in response to changing physiological requirements. This review examines the newly discovered signaling pathways involved in the endocrine functions of bone, such as those mediated by the phosphaturic and 1,25(OH)2D-regulating hormone FGF23, and the broader systemic effects associated with abnormalities of calcium and phosphate homeostasis.
L. Darryl Quarles
Original citation: J. Clin. Invest.118:3820-3828 (2008). doi:10.1172/JCI36479.
Citation for this corrigendum: J. Clin. Invest.119:421 (2009). doi:10.1172/JCI36479C1.
The author wishes to clarify that heterozygous mutations in the SCL34A1 gene have been described in only 2 individuals with nephrolithiasis, renal phosphate loss, and hypophosphatemia (Prié, D., et al. 2002. Nephrolithiasis and osteoporosis associated with hypophosphatemia caused by mutations in the type 2a sodium-phosphate cotransporter. N. Engl. J. Med.347:983–991).
After acceptance of this JCI Science in Medicine article for publication, 3 distinct mutations in NHERF1 were reported in 7 patients with renal phosphate loss and nephrolithiasis and/or bone demineralization (Karim, Z., et al. 2008. NHERF1 mutations and responsiveness of renal parathyroid hormone. N. Engl. J. Med.359:1128–1135).