NT-3 as an upstream and potentially master regulator promoting bone fracture healing

NT-3作为促进骨折愈合的上游和潜在的主调节因子

• 批准号: nhmrc : 1127396
• 负责人: A/Pr Bruce Foster
• 金额: $ 48.66万
• 依托单位: University of South Australia
• 依托单位国家: 澳大利亚
• 项目类别: Project Grants
• 财政年份: 2017
• 资助国家: 澳大利亚
• 起止时间: 2017-01-01 至 2018-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/nt-3-an-fracture-healing/948013
• 关键词: NT; upstream; potentially; master; regulator

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.

对于延迟愈合或骨不连的骨折，临床上强烈需要具有成本效益的治疗方法。我们最近的数据表明，损伤部位来源的神经营养素-3（NT-3）可能是一个重要的整体调节骨修复诱导关键因素参与骨折骨痂形成和重塑。本项目将探讨内源性NT-3在骨修复中的作用和机制，以及外源性NT-3蛋白在临床相关骨折模型中促进骨愈合的可能性。