Autophagy and apoptosis: regulatory factors of chondrocyte phenotype transition in osteoarthritis

被引:15
作者
Liu, Zhibo [1 ]
Wang, Ting [1 ]
Sun, Xianding [1 ]
Nie, Mao [1 ]
机构
[1] Chongqing Med Univ, Ctr Joint Surg, Dept Orthoped Surg, Affiliated Hosp 2, 76 Linjiang Rd, Chongqing, Peoples R China
关键词
Osteoarthritis; Phenotype; Metabolism; Hypertrophic; Senescence; POSTTRAUMATIC OSTEOARTHRITIS; AMELIORATES OSTEOARTHRITIS; SENESCENT CELLS; HYPERTROPHY; ACTIVATION; PROMOTES; PATHOGENESIS; PROGRESSION; PATHWAY;
D O I
10.1007/s13577-023-00926-2
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Osteoarthritis (OA) is the main pathogenic factor in diseases that cause joint deformities. As the main manifestation of the progress of OA, cartilage degradation has been closely associated with the degeneration of chondrocytes, which is induced by inflammatory factors and other trauma factors. Autophagy and apoptosis are the main mechanisms for cells to maintain homeostasis and play crucial roles in OA. Under the influence of external environmental factors (such as aging and injury), the metabolism of cells can be altered, which may affect the extent of autophagy and apoptosis. With the progression of OA, these changes can alter the cell phenotypes, and the cells of different phenotypes display distinct differences in morphology and function. In this review, we have summarized the alteration in cell metabolism, autophagy, and the extent of apoptosis during OA progression and its effects on the cell phenotypes to provide new ideas for further research on the mechanisms of phenotypic transition and therapeutic strategies so as to reverse the cell phenotypes.
引用
收藏
页码:1326 / 1335
页数:10
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