CAJ | 학술논문

背景：软骨细胞的凋亡最终会导致骨关节炎的发生。目前发现的软骨细胞凋亡机制有很多，但内质网应激引起其凋亡的机制尚处于初始阶段。目的：综述分析内质网应激如何引起软骨细胞凋亡，并探寻骨关节炎治疗的新方法。方法：第一作者通过计算机检索，检索了PubMed、CNKI、万方数据库2000年1月至2015年1月的相关文献。使用PubMed检索时，输入检索词“endoplasmic reticulum stress，chondrocyte，apoptosis”之间以“AND”形式连接，使用CNKI、万方数据库检索时，输入主题词“内质网应激，软骨细胞，凋亡”之间以“并且/与”连接，选择模糊查询进行检索。选择文章内容涉及骨关节炎的文献，较多采用近期发表在权威杂志上的相关文献。结果与结论：初检得到中英文文献共计62篇，其中57篇符合纳入标准，对其进行综述。PERK、IRE1和ATF6三条信号通路对软骨细胞同样有重要作用。内质网应激介导的细胞凋亡机制有未折叠蛋白质反应和Ca2+起始信号2种，但具体机制及凋亡途径间的交叉作用还未明了。若从上述信号通路中探索软骨细胞凋亡效应的抑制分子，并将其作为治疗骨关节炎的靶点，可能会为治疗骨关节炎提供新的方法。
배경：연골세포적조망최종회도치골관절염적발생。목전발현적연골세포조망궤제유흔다，단내질망응격인기기조망적궤제상처우초시계단。목적：종술분석내질망응격여하인기연골세포조망，병탐심골관절염치료적신방법。방법：제일작자통과계산궤검색，검색료PubMed、CNKI、만방수거고2000년1월지2015년1월적상관문헌。사용PubMed검색시，수입검색사“endoplasmic reticulum stress，chondrocyte，apoptosis”지간이“AND”형식련접，사용CNKI、만방수거고검색시，수입주제사“내질망응격，연골세포，조망”지간이“병차/여”련접，선택모호사순진행검색。선택문장내용섭급골관절염적문헌，교다채용근기발표재권위잡지상적상관문헌。결과여결론：초검득도중영문문헌공계62편，기중57편부합납입표준，대기진행종술。PERK、IRE1화ATF6삼조신호통로대연골세포동양유중요작용。내질망응격개도적세포조망궤제유미절첩단백질반응화Ca2+기시신호2충，단구체궤제급조망도경간적교차작용환미명료。약종상술신호통로중탐색연골세포조망효응적억제분자，병장기작위치료골관절염적파점，가능회위치료골관절염제공신적방법。
BACKGROUND:Apoptosis of chondrocytes eventualy leads to osteoarthritis. New studies find many mechanisms of chondrocyte apoptosis, but the mechanism of endoplasmic reticulum stress-induced chondrocyte apoptosis is stil in the first stage. OBJECTIVE: To review how the endoplasmic reticulum stress causes the chondrocyte apoptosis and to explore a new method of treatment for osteoarthritis. METHODS: A computer-based online search of PubMed database, CNKI database and Wangfang database between January 2000 and January 2015 was performed to search related articles with the key words of “endoplasmic reticulum stress, chondrocyte, apoptosis” in English or in Chinese, respectively. The word “AND” was used for the connection between the word retrieval. Literatures related to osteoarthritis were selected; the articles published lately in authoritative journals were preferred. RESULTS AND CONCLUSION: A total of 62 literatures were primarily selected, and 57 documents were involved in result analysis according to inclusion criteria. PERK, IRE1 and ATF6 play an important role in the chondrocytes. Endoplasmic reticulum stress-mediated apoptosis mechanisms include two kinds, UPR and Ca2+start signal, but the specific mechanism and the interactions between apoptosis pathway are unclear. Inhibitory molecules for chondrocyte apoptosis in these signaling pathways as treatment targets for osteoarthritis may provide new methods for the treatment of osteoarthritis.