破骨细胞中的钙信号传导。
Calcium signaling in osteoclasts.
作者信息
Hwang Sung-Yong, Putney James W
机构信息
Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, NIH, Department of Health and Human Services, Research Triangle Park, NC 27709, USA.
出版信息
Biochim Biophys Acta. 2011 May;1813(5):979-83. doi: 10.1016/j.bbamcr.2010.11.002. Epub 2010 Nov 11.
It has long been known that many bone diseases, including osteoporosis, involve abnormalities in osteoclastic bone resorption. As a result, there has been intense study of the mechanisms that regulate both the differentiation and bone resorbing function of osteoclast cells. Calcium (Ca(2+)) signaling appears to play a critical role in the differentiation and functions of osteoclasts. Cytoplasmic Ca(2+) oscillations occur during RANKL-mediated osteoclastogenesis. Ca(2+) oscillations provide a digital Ca(2+) signal that induces osteoclasts to up-regulate and autoamplify nuclear factor of activated T cells c1 (NFATc1), a Ca(2+)/calcineurin-dependent master regulator of osteoclastogenesis. Here we review previous studies on Ca(2+) signaling in osteoclasts as well as recent breakthroughs in understanding the basis of RANKL-induced Ca(2+) oscillations, and we discuss possible molecular players in this specialized Ca(2+) response that appears pivotal for normal bone function. This article is part of a Special Issue entitled: 11th European Symposium on Calcium.
长期以来，人们一直知道许多骨疾病，包括骨质疏松症，都涉及破骨细胞骨吸收异常。因此，人们对调节破骨细胞分化和骨吸收功能的机制进行了深入研究。钙（Ca(2+)）信号似乎在破骨细胞的分化和功能中起关键作用。在RANKL介导的破骨细胞生成过程中会发生细胞质Ca(2+)振荡。Ca(2+)振荡提供了一个数字Ca(2+)信号，该信号诱导破骨细胞上调并自动放大活化T细胞核因子c1（NFATc1），这是一种Ca(2+)/钙调磷酸酶依赖性破骨细胞生成的主要调节因子。在这里，我们回顾了以往关于破骨细胞中Ca(2+)信号的研究以及在理解RANKL诱导的Ca(2+)振荡基础方面的最新突破，并讨论了这种对正常骨功能至关重要的特殊Ca(2+)反应中可能的分子参与者。本文是名为：第11届欧洲钙研讨会的特刊的一部分。
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