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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。
The widespread existence of autophagy in eukaryotic cells, is the basic cell self-protection mechanism. Osteoclasts are myeloid derived, highly differentiated multinucleated giant cells that have a variety of biological functions. Under the action of macrophage colony-stimulating factor and RANKL (receptor activator of NF-κB ligand) secreted by osteoblasts and osteocytes, it can promote the formation of osteoclasts and play a role in regulating and maintaining the normal metabolism of bone. As a key mechanism of maintaining the homeostasis of cells, autophagy also plays an important role in the formation and function of osteocytes. This article aims to summarize the biological role of osteoclasts, summarizes the formation of autophagy on osteoclasts and its biological mechanisms of regulation, and autophagy caused by abnormal bone-related diseases are summarized.