Principal Investigator: Ming Zhao, M.D., Ph.D.,
Research Assistant: Hongbin Liu
Research Assistant: Rongrong Zhang
Our functional studies focus on the molecular mechanisms by which genes of interest are involved in postnatal bone homeostasis, particularly, on their physiophathological roles in osteoporosis.
Osteoporosis is a common skeletal disease that is characterized by progressive and age-dependent bone loss and a consequent increased risk of fragile fractures. Approximately 10 million American women have osteoporosis which causes significant morbidity and mortality. Osteoporosis results from an imbalance where overactive bone resorption exceeds declined bone formation. The most compelling clinical need for osteoporosis, at the present time, is a therapeutic intervention that rebuilds bone that has already been lost, perhaps over decades, by stimulating bone formation, and, can be used in conjunction with inhibitors of bone resorption.
The mechanism for postnatal bone formation, particularly in aging, is of fundamental importance to both basic skeletal biology and clinical management of osteoporosis. Bone morphogenetic protein 2 (BMP2) is known as an extremely important anabolic protein that stimulates osteoblast differentiation and bone formation. However, the precise transcriptional mechanisms that control BMP2 expression in osteoblast cells, particularly during skeletal aging warrant further exploration. Recently, we have identified multiple signaling pathways as important mechanisms responsible for BMP2 gene regulation in osteoblasts. Currently, we are conducting the following studies to fully characterize the roles of these signaling pathways in maintenance of postnatal bone mass through regulating osteoblastogenesis and osteoclastogenesis.