4.6 Review

Osteocyte apoptosis

期刊

BONE
卷 54, 期 2, 页码 264-271

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.bone.2012.11.038

关键词

Osteocytes; Apoptosis; RANKL; Mechanical force; Ovariectomy; Glucocorticoid excess

资金

  1. Biomedical Laboratory Research and Development Service of the Veterans Affairs Office of Research and Development [I01 BX000514, I01 BX000436]
  2. National Institutes of Health [P01 AG013918]
  3. UAMS College of Medicine
  4. Medical Research Council [G9321536]

向作者/读者索取更多资源

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.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.6
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据