Protection From Glucocorticoid-Induced Osteoporosis by Anti-Catabolic Signaling in the Absence of Sost/Sclerostin.

ABSTRACT: Excess of glucocorticoids, either due to disease or iatrogenic, increases bone resorption and decreases bone formation and is a leading cause of osteoporosis and bone fractures worldwide. Improved therapeutic strategies are sorely needed. We investigated whether activating Wnt/β-catenin signaling protects against the skeletal actions of glucocorticoids, using female mice lacking the Wnt/β-catenin antagonist and bone formation inhibitor Sost. Glucocorticoids decreased the mass, deteriorated the microarchitecture, and reduced the structural and material strength of bone in wild-type (WT), but not in Sost^-/- mice. The high bone mass exhibited by Sost^-/- mice is due to increased bone formation with unchanged resorption. However, unexpectedly, preservation of bone mass and

SUBMITTER: Sato AY 

PROVIDER: S-EPMC8499032 | biostudies-literature | 2016 Oct

REPOSITORIES: biostudies-literature