激素性骨质疏松症发病机制的研究进展

Research progress of pathogenesis in glucocorticoid-induced osteoporosis

激素性骨质疏松症是临床使用糖皮质激素后常见的副作用,对于激素性骨质疏松的发病机制,从信号通路的层面研究来看,糖皮质激素可以通过抑制骨形成的Wnt/β-catenin、BMPs等信号通路和促进骨吸收的OPG/RANKL/RANK等信号通路引起骨质疏松。近年来对自噬通路和非编码RNA等通路调节因子的研究发现其对激素性骨质疏松的形成有着重要的作用,而且部分通路间的交联反应也被证实是激素性骨质疏松发生的介导因素,这为激素性骨质疏松发病机制的研究提供了新的方向。但是,我们目前的研究层面很可能只是这个复杂的调控网络中的冰山一角,许多通路和调节因子的研究仍处于起步阶段,具体机制很多未完全阐明,仍需要更多的基础和临床实验去完善这个调控网络。本文拟对激素性骨质疏松的发病信号通路及相关通路调节因子研究现状进行综述,为该疾病的靶向治疗提供新的研究方向。

Glucocorticoid-induced osteoporosis is a common side-effect after using glucocorticoid in clinic. At research level of signal pathway,as regards to the pathogenesis of glucocorticoid-induced osteoporosis,glucocorticoid not only inhibits bone formation through Wnt/β-catenin,BMPs,and other classical pathways,but also accelerates bone resorption through OPG/RANKL/RANK and other classical pathways and causes osteoporosis. In recent years,the autophagy pathway and non-coding RNA are confirmed to play a significant role in the development of glucocorticoid-induced osteoporosis,and the crosstalk among the signal pathways also induces glucocorticoid-induced osteoporosis. This provides a new research direction in the pathogenesis of glucocorticoid-induced osteoporosis. However,our current research may be just the top of iceberg of this complex regulatory network. The study of many pathways and regulatory factors are still at the beginning. Many mechanisms are unclear. It needs more basic and clinical trials to improve the regulatory network. The review summarizes the advance of pathogenesis of signal pathways and related regulatory factor in glucocorticoid-induced osteoporosis,aiming to provide a more accurate direction in targeted therapy.