Fibulin2: a negative regulator of BMSC osteogenic differentiation in infected bone fracture healing

Abstract

Bone fracture: Identifying a protein that hinders repair during infection A protein that is overexpressed during bone fracture infection blocks a key signaling pathway and prevents bone repair. Infection following bone fracture remains a leading cause of delayed or unsuccessful healing. Stem cells from bone marrow are the main source of osteoblasts, bone-forming cells necessary for healthy bone regeneration and repair. Infection causes disruption to stem cell function and hinders bone healing, but the exact mechanisms involved remain unclear. In experiments on human tissue samples and a mouse model, Jun Fei and Xiang Xu at the Army Medical University in Chongqing, China, and co-workers examined the role of the fibulin2 protein in infected bone fractures. Fibulin2 is overexpressed in infected tissues, and the protein suppresses stem cell differentiation into osteoblasts by deactivating a key signaling pathway. Blocking fibulin2 in mice models restored bone formation.