间隙连接蛋白-43调控骨组织细胞间平衡在激素性股骨头坏死中的研究进展

Research progress of connexin 43 regulating intercellular balance of bone tissue in glucocorticoids-induced osteonecrosis of the femoral head

摘要:

股骨头坏死是一种以股骨头内成骨细胞（osteoblast，OB）成骨活性降低，破骨细胞（osteoclast，OC）破骨活性增大，骨髓基质干细胞（bone marrow stromal cells，BMSCs）成骨分化降低、成脂分化增强，血管内皮细胞（endothelial cell，EC）受损、血供减少，致使股骨头内骨代谢处于负平衡状态的一种骨代谢疾病。股骨头坏死与骨组织细胞间信息传递异常密切相关。缝隙连接（gap junction，GJ）是相邻细胞间进行信息传递的一种膜通道结构，GJ在骨组织细胞间物质及信号传导通讯中起重要调控作用。通过GJ进行缝隙连接细胞通讯对上述骨代谢动态平衡具有重要作用；间隙连接蛋白-43（connexin 43，Cx43）是骨组织GJ中的重要组分。因此，GJ介导的细胞间信息传递与股骨头坏死等骨代谢疾病的发生密切相关。本文从GJ及Cx43在激素性股骨头坏死疾病中的研究进展作一综述。

Abstract:

Osteonecrosis of femoral head (ONFH), a kind of bone metabolic disease, is featured by reduced osteogenic activity of osteoblasts (OB), increased osteoclast activity of osteoclasts (OC), decreased bone marrow stromal cells (BMSCs) osteogenic differentiation with enhanced adipogenic differentiation, disrupted vascular endothelial cells, and dropped blood supply, resulting in a negative balance of bone metabolism in the femoral head. ONFH is closely related to the abnormal intercellular communication of bone tissue. Gap junction (GJ) is a membrane channel structure for intercellular communication between adjacent cells, and GJ plays an important regulatory role in substance exchange and signal transduction between bone tissue and cells. Communication of gap junction cell through GJ plays an important role to keep the dynamic balance of bone metabolism. Connexin 43 (Cx43) is an important component of GJ in bone tissue. Therefore, GJ-mediated intercellular communication is closely related to the occurrence of bone metabolic diseases such as ONFH. This paper reviews the research progress of GJ and Cx43 roles in the diseases of glucocorticoids-induced ONFH.