Does the downregulation of the FGF23 signaling pathway in hyperplastic parathyroid glands contribute to refractory secondary hyperparathyroidism in CKD patients?
Compared to normal tissue, hyperplastic parathyroid glands of patients with chronic kidney disease on dialysis express lower levels of FGFR1 and Klotho proteins. Similar findings are reported in uremic rats with advanced chronic kidney disease. Moreover, in these animals, FGF23 administration fails to reduce PTH serum levels in vivo and to transmit downstream signals in parathyroid cells ex vivo. These findings may explain, at least partly, the concomitant elevation of both FGF23 and PTH serum levels in chronic kidney disease secondary hyperparathyroidism.
Université de Lyon, Institut National de la Santé et de la Recherche Medical (INSERM) 890, CHU, Saint-Etienne, France. lafagemh@univ-st-etienne.fr
Marie-Hélène
MH
Lafage-Proust
D015536:Down-Regulation; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000378:metabolism* / Q000473:pathology; D007676:Kidney Failure, Chronic / Q000150:complications*; D008954:Models, Biological; D010280:Parathyroid Glands / Q000378:metabolism*; D010281:Parathyroid Hormone / Q000378:metabolism; D015398:Signal Transduction
C000717427:FGF23 protein, human; D010281:Parathyroid Hormone; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23