Regulatory signaling pathways of osteoblast autophagy in periprosthetic osteolysis

YingChu Gu, ZeRui Wu, Heng Xie, Tao Fang, Qiufei Wang, Ye Gu
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Abstract

Periprosthetic osteolysis is a difficult-to-treat complication of arthroplasty. The pathological mechanisms of periprosthetic osteolysis are mainly weakened function of osteoblasts and excessive activation of osteoclasts. Many studies have demonstrated that the imbalance between the formation of bone by osteoblasts and the absorption of bone by osteoclasts is the direct cause of osteolytic diseases. Autophagy, as an important self-protective cellular mechanism, has significant effects on the regulation of osteoblast function, such as osteoblast differentiation, proliferation, and apoptosis. Osteoblasts, which play an important role in maintaining bone homeostasis, have attracted increasing attention in recent years. Up till now, Several signaling pathways have been proved to regulate autophagy of osteoblasts, including the AMPK, NF-κB, FoxO3 and other signaling pathways. This article reviews the recent progress in understanding osteoblast autophagy and mitophagy in the context of periprosthetic osteolysis and the signaling pathways which are involved in these processes. By summarizing previous studies describing the mechanism underlying osteoblast autophagy, we wish to contribute new therapeutic ideas and potential therapeutic targets for periprosthetic osteolysis.
假体周围溶骨过程中成骨细胞自噬的调控信号通路
假体周围溶骨是关节置换术中一种难以治疗的并发症。假体周围溶骨的病理机制主要是成骨细胞功能减弱和破骨细胞过度激活。许多研究表明,成骨细胞形成骨与破骨细胞吸收骨之间的失衡是溶骨性疾病的直接原因。自噬作为一种重要的细胞自我保护机制,对调控成骨细胞的功能,如成骨细胞分化、增殖和凋亡有重要影响。成骨细胞在维持骨稳态中发挥着重要作用,近年来已引起越来越多的关注。迄今为止,已有多种信号通路被证实可调控成骨细胞的自噬,包括 AMPK、NF-κB、FoxO3 等信号通路。本文综述了在假体周围溶骨背景下了解成骨细胞自噬和有丝分裂的最新进展,以及参与这些过程的信号通路。通过总结以往描述成骨细胞自噬机制的研究,我们希望为假体周围骨溶解症提供新的治疗思路和潜在的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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