[HTML][HTML] Turning over renal osteodystrophy dogma: direct actions of FGF23 on osteoblast β-catenin pathway

SC Schiavi, RMA Moysés - Kidney International, 2016 - Elsevier
SC Schiavi, RMA Moysés
Kidney International, 2016Elsevier
Although recognized as a major complication of chronic kidney disease (CKD), the
pathophysiology of the CKD-related mineral and bone disorder (CKD-MBD) is not
completely understood. Recently, the inhibition of Wnt/β-catenin pathway in osteocytes by
sclerostin has been shown to play a role in CKD-MBD. The study by Carrilo-Lopez et al.
confirms this inhibition in an experimental model of CKD. Moreover, they describe direct
actions of FGF23-Klotho on osteoblasts, increasing the expression of DKK1, another Wnt/β …
Although recognized as a major complication of chronic kidney disease (CKD), the pathophysiology of the CKD-related mineral and bone disorder (CKD-MBD) is not completely understood. Recently, the inhibition of Wnt/β-catenin pathway in osteocytes by sclerostin has been shown to play a role in CKD-MBD. The study by Carrilo-Lopez et al. confirms this inhibition in an experimental model of CKD. Moreover, they describe direct actions of FGF23-Klotho on osteoblasts, increasing the expression of DKK1, another Wnt/β-catenin pathway inhibitor.
Elsevier