Using genetic knockout mice as animal models, we investigated into the molecular mechanism underlying the bone development and remodeling, which involves the coupling of osteoblast and osteoclast differentiation processes. Our research would provide novel insights into the therapeutic strategies of degenerative bone diseases, such as osteoporosis and osteoarthritis.
The senescence of mesenchymal stem cells underlies a variety of aging-related diseases. Recently it is a prevaling strategy to treat these diaseases with senolytic method. We have revealed Foxp1 as a transcription factor in regulating senescence of mesenchymal stem cells（MSC), which is a potential target for the treatment of aging diseases.
Foxp2 regulates anatomical features that may be relevant for vocal behavior and bipedal locomotion.
Foxp1 controls cell fate commitment and senescence of mesenchymal stem cells during skeletal aging
Bone marrow fibrosis with fibrocytic and immunoregulatory responses induced by β-catenin activation in osteoprogenitors
Ablation of Wntless in endosteal niches impairs lymphopoiesis rather than HSC maintenance.
Ectodermal Wnt signaling regulates abdominal myogenesis during ventral body wall development.
Osteoblastic Wnts differentially regulate bone remodeling and the maintenance of bone marrow mesenchymal stem cells.
Wnts-mediated reciprocal regulation between cartilage and bone development during endochondral ossification.