Identification and functional analysis of a novel substrate of Pdk4 in the regulation of osteoclastogenesis in the unloaded condition

运动增加骨量，长期卧床、神经损伤导致的制动和空间微重力降低骨量。这些非承重条件导致废用性骨质疏松症。骨细胞网络包埋在骨中，负责感受机械应力并将信号传导至骨表面的成骨细胞和破骨细胞，调节骨量。Pdk4是一种抑制线粒体中能量产生的激酶，在成年小鼠的无负荷条件下在成骨细胞和骨细胞中上调。在Pdk4成年敲除小鼠中未引起无负荷条件下的骨丢失，表明Pdk4参与成年小鼠无负荷条件下的骨丢失。

Bone mass is increase by exercise and reduced by long-term bed rest, immobilization caused by nerve injury, and microgravity in the space. These non-weight bearing conditions cause disuse osteoporosis. Osteocyte network, which is embedded in bone, is responsible for the sensing of mechanical stress and the transduction of the signal to osteoblasts and osteoclasts in the bone surface, and regulates bone mass. Pdk4, which is a kinase that inhibits energy production in mitochondria, was upregulated in osteoblasts and osteocytes in the unloaded condition of adult mice. Bone loss in the unloaded condition was not caused in Pdk4 adult knockout mice, indicating that Pdk4 is involved in bone loss in the unloaded condition of adult mice.