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

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. Aut...

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Bibliographic Details
Published in:Human cell : official journal of Human Cell Research Society 2023-07, Vol.36 (4), p.1326-1335
Main Authors: Liu, Zhibo, Wang, Ting, Sun, Xianding, Nie, Mao
Format: Article
Language:English
Subjects:
Apoptosis
Arthritis
Autophagy
Biomedical and Life Sciences
Cartilage diseases
Cell Biology
Chondrocytes
Cytology
Environmental factors
Gynecology
Homeostasis
Inflammation
Life Sciences
Metabolism
Oncology
Osteoarthritis
Phenotypes
Reproductive Medicine
Review Article
Stem Cells
Surgery
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Summary: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.
ISSN:1749-0774
0914-7470
1749-0774
DOI:10.1007/s13577-023-00926-2