自噬
发病机制
医学
免疫学
类风湿性关节炎
调解人
免疫系统
炎症
细胞生物学
先天免疫系统
关节炎
自身免疫
癌症研究
生物
细胞凋亡
遗传学
出处
期刊:Rheumatology
[Oxford University Press]
日期:2015-09-05
卷期号:: kev337-kev337
被引量:52
标识
DOI:10.1093/rheumatology/kev337
摘要
Autophagy appears to play a dual role in eukaryotic cells. It manifests cytoprotective effects through the regulation of catabolic processes and the clearance of pathogens; however, a correlation between autophagy and the pathogenesis of autoimmune/autoinflammatory conditions has recently been described. Autophagy has emerged as a mediator in the pathogenesis of RA. Autophagy may regulate apoptosis resistance and hyperplasia in synovial fibroblasts, promote osteoclastogenesis and stimulate osteoclast-mediated bone resorption through the delivery of citrullinated peptides to MHC compartments, which results in the activation of the innate and adaptive immune response, thereby resulting in RA. Given the likely importance of autophagy in the pathogenesis of RA, here we reviewed the detailed mechanisms concerning the pathogenicity of autophagy and autophagy proteins in RA.
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