Osteocyte apoptosis.

Osteocyte apoptosis.
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DOI:
10.1016/j.bone.2012.11.038
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发表时间:
2013-06
期刊:
影响因子:
4.1
通讯作者:
Weinstein RS
Weinstein RS
中科院分区:
医学2区
文献类型:
--
作者:
Jilka RL;Noble B;Weinstein RS

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骨细胞凋亡早在15年前就被认识到,但其对骨稳态的意义仍不明确。一种新的范式已经出现,它将骨细胞凋亡作为破骨细胞募集到特定部位的关键事件,以响应骨骼卸载、疲劳损伤、雌激素缺乏以及其他必须去除骨骼的状态。这是通过死亡的骨细胞发出的尚未定义的信号来完成的,这些信号刺激邻近的活骨细胞产生破骨细胞因子。慢性糖皮质激素引起的骨细胞凋亡不增加破骨细胞;然而,它确实对维持骨水化、血管和强度有负面影响。
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.
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