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Osteocyte apoptosis
DOI:10.1016/j.bone.2012.11.038.png)
摘要
En 中文
Apoptotic death of osteocytes was recognized over 15 years ago, but its significance for bone homeostasis has remained elusive. A new paradigm has emerged that invokes osteocyte apoptosis as a critical event in the recruitment of osteoclasts to a specific site in response to skeletal unloading, fatigue damage, estrogen deficiency and perhaps in other states where bone must be removed. This is accomplished by yet to be defined signals emanating from dying osteocytes, which stimulate neighboring viable osteocytes to produce osteoclastogenic cytokines. The osteocyte apoptosis caused by chronic glucocorticoid administration does not increase osteoclasts; however, it does negatively impact maintenance of bone hydration, vascularity, and strength. This article is part of a Special Issue entitled The Osteocyte. Published by Elsevier Inc.
Keyword:
Osteocytes
Apoptosis
RANKL
Mechanical force
Ovariectomy
Glucocorticoid excess
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期刊
IF:
3.6
论文数:
1.3W
被引数:
2.3W
机构
引用论文
Endogenous glucocorticoids decrease skeletal angiogenesis, vascularity, hydration, and strength in aged mice
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