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GDF11 decreases bone mass by stimulating osteoclastogenesis and inhibiting osteoblast differentiation

Osteoporosis is an age-related disease that affects millions of people. Growth differentiation factor 11 (GDF11) is a secreted member of the transforming growth factor beta (TGF-β) superfamily. Deletion of Gdf11 has been shown to result in a skeletal anterior–posterior patterning disorder. Here we s...

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Detalles Bibliográficos
Autores principales: Liu, Weiqing, Zhou, Liyan, Zhou, Chenchen, Zhang, Shiwen, Jing, Junjun, Xie, Liang, Sun, Ningyuan, Duan, Xiaobo, Jing, Wei, Liang, Xing, Zhao, Hu, Ye, Ling, Chen, Qianming, Yuan, Quan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5036163/
https://www.ncbi.nlm.nih.gov/pubmed/27653144
http://dx.doi.org/10.1038/ncomms12794
Descripción
Sumario:Osteoporosis is an age-related disease that affects millions of people. Growth differentiation factor 11 (GDF11) is a secreted member of the transforming growth factor beta (TGF-β) superfamily. Deletion of Gdf11 has been shown to result in a skeletal anterior–posterior patterning disorder. Here we show a role for GDF11 in bone remodelling. GDF11 treatment leads to bone loss in both young and aged mice. GDF11 inhibits osteoblast differentiation and also stimulates RANKL-induced osteoclastogenesis through Smad2/3 and c-Fos-dependent induction of Nfatc1. Injection of GDF11 impairs bone regeneration in mice and blocking GDF11 function prevents oestrogen-deficiency-induced bone loss and ameliorates age-related osteoporosis. Our data demonstrate that GDF11 is a previously unrecognized regulator of bone remodelling and suggest that GDF11 is a potential target for treatment of osteoporosis.