Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD, USA.
Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD, USA.
FEBS Lett. 2014 Apr 17;588(8):1315-21. doi: 10.1016/j.febslet.2014.01.025. Epub 2014 Jan 28.
The role of gap junctions, particularly that of connexin43 (Cx43), has become an area of increasing interest in bone physiology. An abundance of studies have shown that Cx43 influences the function of osteoblasts and osteocytes, which ultimately impacts bone mass acquisition and skeletal homeostasis. However, the molecular details underlying how Cx43 regulates bone are only coming into focus and have proven to be more complex than originally thought. In this review, we focus on the diverse molecular mechanisms by which Cx43 gap junctions and hemichannels regulate cell signaling pathways, gene expression, mechanotransduction and cell survival in bone cells. This review will highlight key signaling factors that have been identified as downstream effectors of Cx43 and the impact of these pathways on distinct osteoblast and osteocyte functions.
缝隙连接,特别是连接蛋白 43(Cx43)的作用,已成为骨生理学中日益受到关注的领域。大量研究表明,Cx43 影响成骨细胞和骨细胞的功能,这最终影响骨量的获得和骨骼的内稳态。然而,Cx43 调节骨骼的分子细节才刚刚开始显现,事实证明比最初想象的要复杂得多。在这篇综述中,我们重点关注 Cx43 缝隙连接和半通道调节骨细胞信号通路、基因表达、机械转导和细胞存活的多种分子机制。这篇综述将重点介绍已被确定为 Cx43 下游效应物的关键信号因子,以及这些途径对不同成骨细胞和骨细胞功能的影响。