Disruption of glucocorticoid signaling in chondrocytes delays metaphyseal fracture healing but does not affect normal cartilage and bone development

States of glucocorticoid excess are associated with defects in chondrocyte function. Most prominently there is a reduction in linear growth but delayed healing of fractures that require endochondral ossification to also occur. In contrast, little is known about the role of endogenous glucocorticoids...

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Foilsithe in:Bone
Main Authors: Tu, Jinwen, Henneicke, Holger, Zhang, Yaqing, Stoner, Shihani, Cheng, Tegan L., Schindeler, Aaron, Chen, Di, Tuckermann, Jan, Cooper, Mark S., Seibel, Markus J., Zhou, Hong
Formáid: Artigo
Teanga:Inglês
Foilsithe: 2014
Ábhair:
Article
Rochtain Ar Líne:https://ncbi.nlm.nih.gov/pmc/articles/PMC4284102/
https://ncbi.nlm.nih.gov/pubmed/25193158
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.bone.2014.08.016
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