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线粒体力学转导与软骨细胞生物学在骨关节炎发病机制中的联系。

Mechanisms linking mitochondrial mechanotransduction and chondrocyte biology in the pathogenesis of osteoarthritis.

机构信息

Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.

Department of Orthopaedics, Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, 646000, China.

出版信息

Ageing Res Rev. 2021 May;67:101315. doi: 10.1016/j.arr.2021.101315. Epub 2021 Mar 5.

DOI:10.1016/j.arr.2021.101315
PMID:33684550
Abstract

Mechanical loading is essential for chondrocyte health. Chondrocytes can sense and respond to various extracellular mechanical signals through an integrated set of mechanisms. Recently, it has been found that mitochondria, acting as critical mechanotransducers, are at the intersection between extracellular mechanical signals and chondrocyte biology. Much attention has been focused on identifying how mechanical loading-induced mitochondrial dysfunction contributes to the pathogenesis of osteoarthritis. In contrast, little is known regarding the mechanisms underlying functional alterations in mitochondria induced by mechanical stimulation. In this review, we describe how chondrocytes perceive environmental mechanical signals. We discuss how mechanical load induces mitochondrial functional alterations and highlight the major unanswered questions in this field. We speculate that AMP-activated protein kinase (AMPK), a master regulator of energy homeostasis, may play an important role in coupling force transmission to mitochondrial health and intracellular biological responses.

摘要

机械加载对于软骨细胞的健康至关重要。软骨细胞可以通过一整套整合机制感知和响应各种细胞外机械信号。最近发现,线粒体作为关键的机械转导器,处于细胞外机械信号和软骨细胞生物学的交汇点。人们越来越关注机械加载诱导的线粒体功能障碍如何导致骨关节炎的发病机制。相比之下,对于机械刺激引起的线粒体功能改变的机制知之甚少。在这篇综述中,我们描述了软骨细胞如何感知环境中的机械信号。我们讨论了机械负荷如何诱导线粒体功能改变,并强调了该领域的主要未解决问题。我们推测,AMP 激活的蛋白激酶(AMPK)作为能量平衡的主要调节剂,可能在将力传递与线粒体健康和细胞内生物反应偶联方面发挥重要作用。

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