背景:虽然骨关节炎(OA)的发展在流行病学上是多因素的,一个主要的潜在机制仍在辩论中。了解OA的病理生理学仍然具有挑战性。最近,专家们一直关注自噬作为OA发展的贡献者。方法:为了更好地了解OA的发病机制,我们综述了自噬的作用和OA发生发展的分子机制的文献。为了确定相关研究,我们使用受控词汇和自由文本关键字来搜索MEDLINE,EMBASE,Cochrane中央受控试验登记册,WebofScience,和SCOPUS数据库。纳入31项研究进行数据提取和系统评价。在这些研究中,25项研究调查了自噬在衰老和OA软骨细胞中的作用,六项研究检查了自噬在正常人软骨细胞中的作用,只有一项研究调查了机械应力诱导的自噬对正常软骨细胞OA发展的影响。结果:研究表明,自噬激活通过在正常人软骨细胞中发挥细胞保护作用来预防OA。然而,在老化和骨关节炎(OA)软骨细胞,自噬的作用错综复杂,正如某些研究表明,刺激这些细胞中的自噬可以具有细胞毒性作用,而其他人则认为它可能具有针对损伤或变性的保护(细胞保护)作用。结论:机械应力诱导的自噬也被认为参与了OA的发生发展,但是需要进一步的研究来确定确切的机制。因此,在衰老和OA软骨的类型中,应谨慎解释自噬的贡献。
Background: Although osteoarthritis (OA) development is epidemiologically multifactorial, a primary underlying mechanism is still under debate. Understanding the pathophysiology of OA remains challenging. Recently, experts have focused on
autophagy as a contributor to OA development. Method: To better understand the pathogenesis of OA, we survey the literature on the role of
autophagy and the molecular mechanisms of OA development. To identify relevant studies, we used controlled vocabulary and free text keywords to search the MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials, Web of Science, and SCOPUS database. Thirty-one studies were included for data extraction and systematic
review. Among these studies, twenty-five studies investigated the effects of autophagy in aging and OA chondrocytes, six studies examined the effects of autophagy in normal human chondrocytes, and only one study investigated the effects of mechanical stress-induced
autophagy on the development of OA in normal chondrocytes. Results: The studies suggest that autophagy activation prevents OA by exerting cell-protective effects in normal human chondrocytes. However, in aging and osteoarthritis (OA) chondrocytes, the role of autophagy is intricate, as certain studies indicate that stimulating
autophagy in these cells can have a cytotoxic effect, while others propose that it may have a protective (cytoprotective) effect against damage or degeneration. Conclusions: Mechanical stress-induced autophagy is also thought to be involved in the development of OA, but further research is required to identify the precise mechanism. Thus, autophagy contributions should be interpreted with caution in aging and the types of OA cartilage.