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...

Deskribapen osoa

Gorde:
Xehetasun bibliografikoak
Argitaratua izan da:Bone
Egile Nagusiak: 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
Formatua: Artigo
Hizkuntza:Inglês
Argitaratua: 2014
Gaiak:
Article
Sarrera elektronikoa: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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