自噬
软骨细胞
细胞生物学
骨关节炎
PI3K/AKT/mTOR通路
软骨
医学
程序性细胞死亡
细胞凋亡
活性氧
信号转导
癌症研究
生物
病理
解剖
生物化学
替代医学
作者
Zhihong Li,Fangjie Zhang,Chao Zeng,Wei Luo,Wenfeng Xiao,Shuguang Gao,Guanghua Lei
标识
DOI:10.1016/j.jbspin.2015.06.009
摘要
Degradation of the articular cartilage is at the centre of the pathogenesis of osteoarthritis (OA), for which age is the major risk factor. Maintaining the chondrocytes in a healthy condition appears to be an important factor for preservation of the entire cartilage and preventing its degeneration. Autophagy, which is an essential cellular homeostatic mechanism for the removal of dysfunctional cellular organelles and macromolecules, is increased by catabolic and nutritional stresses. Autophagy is increased in OA chondrocytes and cartilage, particularly during the initial degenerative phase, to regulate changes in OA-like gene expression through modulation of apoptosis and reactive oxygen species (ROS). In this way, autophagy acts as an adaptive response to protect chondrocytes from various environmental changes, while with gradual cartilage degradation, decreased autophagy is linked with cell death. Rapamycin, which is a specific inhibitor of the mTOR signaling pathway, enhances expression of autophagy regulators and prevents chondrocyte death. In the future, pharmacological activation of autophagy may be an effective therapeutic approach for OA.
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