osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification

作者：Nathan Bucay, Ildiko Sarosi, Colin Robert Dunstan, Sean Morony, John E. Tarpley, Charles Capparelli, Sheila A. Scully, Hong‐Lin Tan, Weili Xu, David L. Lacey, W. J. Boyle, W. Scott Simonet · 发表于：Genes & Development · 年份：1998 · DOI：10.1101/gad.12.9.1260 · 被引用次数：2497 · 研究领域：Bone Metabolism and Diseases、Bone health and treatments、Bone health and osteoporosis research

Osteoprotegerin (OPG) is a secreted protein that inhibits osteoclast formation. In this study the physiological role of OPG is investigated by generating OPG-deficient mice. Adolescent and adult OPG-/- mice exhibit a decrease in total bone density characterized by severe trabecular and cortical bone porosity, marked thinning of the parietal bones of the skull, and a high incidence of fractures. These findings demonstrate that OPG is a critical regulator of postnatal bone mass. Unexpectedly, OPG-deficient mice also exhibit medial calcification of the aorta and renal arteries, suggesting that regulation of OPG, its signaling pathway, or its ligand(s) may play a role in the long observed association between osteoporosis and vascular calcification.