国际口腔医学杂志2016，Vol.43Issue(4)：462-467,6.DOI:10.7518/gjkq.2016.04.019
细胞自噬和炎症反应的相互调控与牙周炎
Interaction of autophagy and inflammation in periodontitis
摘要
Abstract
In autophagy, damaged proteins, organelles, and nutrients are transported to lysosomes for degradation, elimination, and recycling. This process is a highly conserved mechanism among eukaryotic cells. Inflammation is a vital protective host response to tissue damage and pathogenic infection. However, excessive inflammation can cause tissue damage and diseases. Autophagy inhibits the assembly of inflammasomes by degrading endogenous stimuli, including DNA and reactive oxygen species. This process also controls interleukin(IL)-1β secretion by targeting pro-IL-1β for degradation. Periodontal pathogens destroy periodontal tissues through the interaction of Toll-like receptor(TLR) with various components, such as lipopolysaccharide, peptidoglycan, and bacterial DNA. As a consequence, inflammatory cells are recruited and inflammatory cytokines are released. In local periodontal tissues, TLR or nucleotide-binding oligomerization domain-like receptor activates innate immune responses, induces autophagy-related pathways, and recognizes pathogen- and damage-associated molecular patterns. Autophagy can also influence inflammatory responses by negatively regulating TLR signals. This review focuses on recent progress in the mutual regulation of autophagy and inflammation. This review also describes the potential relations between autophagy and periodontitis to elucidate disease pathogenesis and to develop new therapies.关键词
自噬/炎症/Toll样受体/牙周炎Key words
autophagy/inflammation/Toll-like receptor/periodontitis分类
医药卫生引用本文复制引用
任静宜,刘歆婵,丁烨,于洪强,周延民,于维先..细胞自噬和炎症反应的相互调控与牙周炎[J].国际口腔医学杂志,2016,43(4):462-467,6.基金项目
吉林省卫生厅资助项目（20102045）；吉林省发改委资助项目（2013C022-4）；吉林省科技厅资助项目 （）
