FGFR antagonists restore defective mandibular bone repair in a mouse model of osteochondrodysplasia  

作　　者：Anne Morice Amélie de La Seiglière Alexia Kany Roman H.Khonsari Morad Bensidhoum Maria-Emilia Puig-Lombardi Laurence Legeai Mallet 

机构地区：[1]Universitéde Paris Cité,Imagine Institute,Laboratory of Molecular and Physiopathological Bases of Osteochondrodysplasia,INSERM UMR 1163,Paris,France [2]B3OA UMR CNRS 7052,UniversitéParis Cité,Paris,France [3]Bioinformatics Core Platform,Imagine Institute,INSERM UMR1163 and Structure Fédérative de Recherche Necker,INSERM US24/CNRS UAR3633,UniversitéParis Cité,Paris,France

出　　处：《Bone Research》2025年第1期197-211,共15页骨研究(英文版)

基　　金：National Research Agency under the Investments for the Future program (ANR-10-IAHU-01);Filière Nationale TeteCou for financial support。

摘　　要：Gain-of-function mutations in fibroblast growth factor receptor(FGFR) genes lead to chondrodysplasia and craniosynostoses. FGFR signaling has a key role in the formation and repair of the craniofacial skeleton. Here, we analyzed the impact of Fgfr2- and Fgfr3- activating mutations on mandibular bone formation and endochondral bone repair after non-stabilized mandibular fractures in mouse models of Crouzon syndrome(Crz) and hypochondroplasia(Hch).

关 键 词：MANDIBULAR DYSPLASIA facial 

分 类 号：R78[医药卫生—口腔医学]