Sclerostin, a well-known inhibitor of physiological bone formation, protects against vascular calcification development in mice. A significantly increased calcium content was observed in: (i) cardiac vessels of Sost^−/− mice versus WT mice, after induction of renal failure and (ii) aorta and renal vessels of anti-sclerostin antibody-treated versus vehicle-treated mice.

Reconstructions of representative T2DM cancellous specimen with highlighted plate microdamage (green) and rod microdamage (red). Rods were more damaged relative to their volume vs. plates in non-DM specimens but this difference was absent in T2DM specimens.