Huzhou Central Hospital, 313000, Huzhou, People's Republic of China.
Int Orthop. 2021 May;45(5):1125-1136. doi: 10.1007/s00264-021-04938-1. Epub 2021 Jan 18.
Mechanical loading enhances the progression of osteoarthritis. However, its molecular mechanisms have not been established.
The aim of this review was to summarize the probable mechanisms of mechanical load-induced osteoarthritis.
A comprehensive search strategy was used to search PubMed and EMBASE databases (from the 15th of January 2015 to the 20th of October 2020). Search terms included "osteoarthritis", "mechanical load", and "mechanism".
Abnormal mechanical loading activates the interleukin-1β, tumour necrosis factor-α, nuclear factor kappa-B, Wnt, transforming growth factor-β, microRNAs pathways, and the oxidative stress pathway. These pathways induce the pathological progression of osteoarthritis. Mechanical stress signal receptors such as integrin, ion channel receptors, hydrogen peroxide-inducible clone-5, Gremlin-1, and transient receptor potential channel 4 are present in the articular cartilages.
This review highlights the molecular mechanisms of mechanical loading in inducing chondrocyte apoptosis and extracellular matrix degradation. These mechanisms provide potential targets for osteoarthritis prevention and treatment.
机械负荷可促进骨关节炎的进展。然而，其分子机制尚未确定。
本综述旨在总结机械负荷诱导骨关节炎的可能机制。
采用全面的检索策略，检索了 PubMed 和 EMBASE 数据库（2015 年 1 月 15 日至 2020 年 10 月 20 日）。检索词包括“骨关节炎”、“机械负荷”和“机制”。
异常的机械负荷会激活白细胞介素-1β、肿瘤坏死因子-α、核因子 kappa-B、Wnt、转化生长因子-β、微小 RNA 通路和氧化应激通路。这些通路诱导骨关节炎的病理进展。整合素、离子通道受体、过氧化氢诱导克隆-5、Gremlin-1 和瞬时受体电位通道 4 等机械应激信号受体存在于关节软骨中。
本综述强调了机械负荷诱导软骨细胞凋亡和细胞外基质降解的分子机制。这些机制为骨关节炎的预防和治疗提供了潜在的靶点。
