自噬在破骨细胞中的调控作用

The regulation function of autophagy in osteoclast

自噬广泛存在于真核细胞中,是细胞基本的自我保护机制。破骨细胞是髓系来源的高度分化的多核巨细胞,具有多种生物学功能。在成骨细胞和骨细胞分泌的巨噬细胞集落刺激因子和RANKL(receptor activator of NF-κB ligand)的作用下,可促进破骨细胞的形成,对调控和维持骨骼正常代谢发挥作用。自噬作为保守的维持细胞稳态的重要作用机制,同样在骨细胞的形成和功能发挥过程中起着重要的作用。本文旨在总结破骨细胞的生物学作用,概括自噬对破骨细胞的形成及对其生物学作用的调控机制,并对自噬异常造成的骨相关疾病进行总结。

Autophagy, a cellular self-protection mechanism, exists in all eukaryocytes. Originated from bone marrow stem cells, osteoclasts are armed with multiple biological functions. Osteoclasts formation are promoted by macrophage colony-stimulating factor and receptor activator of NF-κB ligand（RANKL） secreted by osteoblasts and osteocytes, which are essential in regulating and maintaining the normal metabolism of bones. As a conservative fundamental mechanism to maintain cellular homeostasis, autophagy is also critical for the forming and function of osteoclasts. Our review will discuss the regulation of autophagy on biological function of osteoclasts and underlying mechanisms, and dysregulation of the autophagic response in the pathogenesis of bone-related disorders will also be included.