自噬基因在骨关节炎软骨细胞凋亡过程中的保护和平衡效应

背景：软骨细胞在低营养供给下可发生细胞自噬，细胞自噬和细胞坏死、凋亡不同，可以使软骨细胞在营养供给不足时，能够存活下来，可能是软骨细胞自身的重要保护机制之一。 目的：综合阐述自噬基因保护关节软骨及抑制骨关节炎等方面的机制和作用。 方法：应用计算机检索中国知网、万方数据库及PubMed数据库2000年1月至2015年1月关于自噬基因与骨关节炎的相关研究的文章，中文检索词为“自噬基因、骨关节炎、关节软骨、软骨细胞”，英文检索词为“autophagy、osteoarthritis、beclin1、LC3”。选择自噬基因与骨关节炎的相关文章，初检得到269余篇文献，根据纳入标准选择其中的38篇进行综述。  结果与结论：软骨细胞的损伤凋亡是软骨退变的主要机制，不予控制，就可能会进一步发展为骨性关节炎。细胞的损伤凋亡是软骨退变的重要机制之一，因此防止软骨细胞的损伤凋亡，可能有利于损伤软骨的修复，以此来缓解骨关节炎的病情发展。自噬现象能够抑制受损软骨细胞凋亡，发现其可将改变传统治疗骨关节炎的局限，但目前自噬基因与骨关节炎相关的研究还处于初级阶段，特别是对自噬途径在软骨中如何被诱导，如何进行信号转导，如何对软骨细胞生存产生影响等方面的认识还不够全面，有待进一步的研究。

Autophagy genes associated with chondrocyte apoptosis: protection and balancing effects

BACKGROUND:Autophagy can occur in chondrocytes under the low supply of nutrients. Different from necrosis and apoptosis, autophagy can make chondrocytes survive in insufficient supply of nutrients, which may be an important mechanism for the self-protection of chondrocytes. OBJECTIVE:To review the mechanism and effect of autophagy gene to protect the articular cartilage and inhibit osteoarthritis. METHODS:A computer-based search was perform in CNKI, Wanfang, PubMed to retrieve articles addressing autophagy gene and osteoarthritis published from January 2000 to January 2015. The keywords were “autophagy, osteoarthritis, articular cartilage, chondrocytes” in Chinese and “autophagy, osteoarthritis, beclin1, LC3” in English. Totally 269 articles were initially searched, and finally, 38 articles were included in result analysis.  RESULTS AND CONCLUSION:Apoptosis of damaged chondrocytes is the main mechanism of articular cartilage degeneration, which can further develop into osteoarthritis. The damage and death of cells is one of the important mechanisms of cartilage degeneration, thus, to prevent damaged chondrocyte apoptosis may help cartilage repair, thus alleviating the progression of osteoarthritis. Autophagy can inhibit damaged chondrocyte apoptosis, which changes the limitations of traditional treatments for osteoarthritis. However, the current research on autophagy genes associated with osteoarthritis is still at the primary stage, and further studies are needed on how to induce authopagy pathway in the cartilage, how to do the signal transduction and how to have an effect on the survival of chondrocytes.