NT-3 As An Upstream And Potentially Master Regulator Promoting Bone Fracture Healing
Funder
National Health and Medical Research Council
Funding Amount
$712,857.00
Summary
There is a strong clinical need for cost-effective treatments for delayed healing or non-union bone fractures. Our recent data suggest injury site-derived neurotrophin-3 (NT-3) may be an important overall regulator of bone repair by inducing key factors involved in fracture callus formation and remodelling. This project will address roles and mechanisms of endogenous NT-3 in bone repair and the likelihood of exogenous NT-3 protein in promoting bone healing in clinically relevant fracture models.