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Cortical bone loss caused by glucocorticoid excess requires RANKL production by osteocytes and is associated with reduced OPG expression in mice
Glucocorticoid excess is a major cause of low bone mass and fractures. Glucocorticoid administration decreases cortical thickness and increases cortical porosity in mice, and these changes are associated with increased osteoclast number at the endocortical surface. Receptor activator of NF-κB ligand...
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| Pubblicato in: | Am J Physiol Endocrinol Metab |
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| Autori principali: | , , , , |
| Natura: | Artigo |
| Lingua: | Inglês |
| Pubblicazione: |
American Physiological Society
2016
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| Soggetti: | |
| Accesso online: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5142003/ https://ncbi.nlm.nih.gov/pubmed/27460899 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1152/ajpendo.00219.2016 |
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