Osteoporosis and osteoporotic fractures lead to decreased life quality and high healthcare costs. Current treatments prevent losses in bone mass and fractures to some extent but have side effects. Therefore, better therapies are needed. This study investigated whether the transcription factor Jun has a specific pro-osteogenic potency and whether modulating Jun could serve as a novel treatment for osteoporosis-associated fractures. We demonstrate that ectopically transplanted whole bones and distinct osteoprogenitors increase bone formation. Perinatal Jun induction disturbs growth plate architecture, causing a striking phenotype with shortened and thickened bones. Molecularly, Jun induces hedgehog signaling in skeletal stem cells. Therapeutically, Jun accelerates bone growth and healing in a drilling-defect model. Altogether, these results demonstrate that Jun drives bone formation by expanding osteoprogenitor populations and forcing them into the bone fate, providing a rationale for future clinical applications.

骨质疏松症和骨质疏松性骨折会导致生活质量下降和医疗费用高昂。目前的治疗在一定程度上防止了骨量和骨折的损失，但有副作用。因此，需要更好的疗法。本研究调查了转录因子 Jun 是否具有特定的促成骨效力，以及调节 Jun 是否可以作为骨质疏松症相关骨折的新疗法。我们证明异位移植的全骨和不同的骨祖细胞会增加骨形成。围产期 Jun 诱导扰乱了生长板结构，导致骨骼缩短和增厚的显着表型。在分子上，Jun 在骨骼干细胞中诱导刺猬信号。在治疗上，Jun 在钻孔缺陷模型中加速骨骼生长和愈合。共，