A soluble activin type IIA receptor induces bone formation and improves skeletal integrity

作者：Pearsall R Scott^*; C****is Ernesto; Cornwall Brady Milton; Underwood Kathryn W; Haigis Brendan; Ucran Jeffrey; Kumar Ravindra; Pobre Eileen; Grinberg Asya; Werner Eric D; Glatt Vaida; Stadmeyer Lisa; Smith Deanna; Seehra Ja**ir; Bouxsein Mary L

来源：Proceedings of the National Academy of Sciences, 2008, 105(19): 7082-7087.

DOI：10.1073/pnas.0711263105

• anabolic
• osteoporosis
• TGF-beta
• therapeutic

Diseases that affect the regulation of bone turnover can lead to skeletal fragility and increased fracture risk. Members of the TGF-beta superfamily have been shown to be involved in the regulation of bone mass. Activin A, a TGF-beta signaling ligand, is present at high levels in bone and may play a role in the regulation of bone metabolism. Here we demonstrate that pharmacological blockade of ligand signaling through the high affinity receptor for activin, type II activin receptor (ActRIIA), by administration of the soluble extracellular domain of ActRIIA fused to a murine IgG2a-Fc, increases bone formation, bone mass, and bone strength in normal mice and in ovariectomized mice with established bone loss. These observations support the development of this pharmacological strategy for the treatment of diseases with skeletal fragility.

• 出版日期2008-5-13