Bone metabolic disorders include osteolysis, osteoporosis, osteoarthritis and rheumatoid arthritis. Osteoblasts and osteoclasts are two major types of cells in bone constituting homeostasis. The imbalance between bone formation by osteoblasts and bone resorption by osteoclasts has been shown to have a direct contribution to the onset of these diseases. Recent evidence indicates that autophagy and mitophagy, the selective autophagy of mitochondria, may play a vital role in regulating the proliferation, differentiation and function of osteoblasts and osteoclasts. Several signaling pathways, including PINK1/Parkin, SIRT1, MAPK8/FOXO3, Beclin-1/BECN1, p62/SQSTM1, and mTOR pathways, have been implied in the regulation of autophagy and mitophagy in these cells. Here we review the current progress about the regulation of autophagy and mitophagy in osteoblasts and osteoclasts in these bone metabolic disorders, as well as the molecular signaling activated or deactivated during this process. Together, we hope to draw attention to the role of autophagy and mitophagy in bone metabolic disorders, and their potential as a new target for the treatment of bone metabolic diseases and the requirements of further mechanism studies.

中文翻译：

---

自噬和线粒体自噬在骨代谢疾病中的作用。

骨代谢紊乱包括骨质溶解、骨质疏松、骨关节炎和类风湿性关节炎。成骨细胞和破骨细胞是构成体内平衡的骨骼中的两种主要细胞类型。成骨细胞的骨形成与破骨细胞的骨吸收之间的不平衡已被证明对这些疾病的发生有直接影响。最近的证据表明，自噬和线粒体自噬，即线粒体的选择性自噬，可能在调节成骨细胞和破骨细胞的增殖、分化和功能方面发挥重要作用。几种信号通路，包括 PINK1/Parkin、SIRT1、MAPK8/FOXO3、Beclin-1/BECN1、p62/SQSTM1 和 mTOR 通路，已被暗示在这些细胞的自噬和线粒体自噬的调节中。在这里，我们回顾了这些骨代谢疾病中成骨细胞和破骨细胞中自噬和线粒体自噬调节的当前进展，以及在此过程中激活或失活的分子信号传导。我们希望共同关注自噬和线粒体自噬在骨代谢疾病中的作用，以及它们作为骨代谢疾病治疗新靶点的潜力以及进一步机制研究的需求。