Molecular mechanisms of autophagy-apoptosis interactions in osteoarthritis
- VernacularTitle:骨关节炎中自噬与凋亡相互作用的分子机制
- Author:
Kui ZHAO
1
;
Runsang PAN
;
Fengjun LAN
;
Jin DENG
;
Houping CHEN
Author Information
- Keywords: osteoarthritis; chondrocyte; joint degeneration; autophagy; apoptosis; signaling pathway
- From: Chinese Journal of Tissue Engineering Research 2024;28(18):2912-2917
- CountryChina
- Language:Chinese
- Abstract: BACKGROUND:With the deepening of the aging of the world population,the prevalence rate of osteoarthritis is increasing.In recent years,more and more attention has been paid to the study of osteoarthritis.Studies have shown that autophagy and apoptosis are strongly associated with the occurrence and development of osteoarthritis,and play an important role in it. OBJECTIVE:To review the molecular mechanisms of the interaction between autophagy and apoptosis in osteoarthritis,aiming to explore the relationship between autophagy and apoptosis in osteoarthritis and the coupling mechanism of the two to mediate the occurrence and development of osteoarthritis,so as to provide new ideas for the treatment of osteoarthritis. METHODS:The Chinese and English key words"osteoarthritis,autophagy,apoptosis"were searched in the CNKI and PubMed.After screening by reading the title,abstract and key words,the relevant literature was carefully read.After excluding studies unrelated to the content of the paper and repetitive studies,68 articles were finally included for the summary. RESULTS AND CONCLUSION:(1)The occurrence and development of osteoarthritis are related to autophagy and apoptosis of chondrocytes.Autophagy protects chondrocytes from stress damage,but excessive autophagy also induces or promotes chondrocyte apoptosis and reduces the survival rate of chondrocytes.The two perturb each other to regulate the degeneration of articular cartilage.(2)miRNA,Beclin-1 and oxidative stress are all involved in the regulation of autophagy and apoptosis on osteoarthritis,and affect the development of osteoarthritis.
