Regulation of apoptosis and interaction with cartilage degeneration in osteoarthritis
Osteoarthritis (OA) is a chronic degenerative joint disease, primarily characterized by the degradation of the ECM and cartilage degeneration. Articular cartilage is maintained by chondrocytes, which secrete the ECM, making the stability of these cells crucial for joint function. Research has shown...
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| Format: | Article |
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Frontiers Media S.A.
2025-03-01
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| Series: | Frontiers in Cell and Developmental Biology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fcell.2025.1571448/full |
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| author | Jiahua Mei Niqin Xiao Yujiang Xi Xin Chen Xuezhi Zha Lili Cui Fei Yan Rui Xue Yongsen Wang Yunshu Ma Yunshu Ma Yunshu Ma |
| author_facet | Jiahua Mei Niqin Xiao Yujiang Xi Xin Chen Xuezhi Zha Lili Cui Fei Yan Rui Xue Yongsen Wang Yunshu Ma Yunshu Ma Yunshu Ma |
| author_sort | Jiahua Mei |
| collection | DOAJ |
| description | Osteoarthritis (OA) is a chronic degenerative joint disease, primarily characterized by the degradation of the ECM and cartilage degeneration. Articular cartilage is maintained by chondrocytes, which secrete the ECM, making the stability of these cells crucial for joint function. Research has shown that in the later stages of OA, cartilage cavities form, indicating a decline in chondrocyte function. Chondrocyte death is considered a central feature of cartilage degeneration. Apoptosis, a form of programmed cell death, plays a key role in this process. While controlled apoptosis helps remove damaged chondrocytes and protects the cartilage from injury, excessive apoptosis disrupts the balance of the cartilage microenvironment and accelerates OA progression. Therefore, regulating chondrocyte apoptosis may offer a novel approach for preventing and treating cartilage degeneration. This review examines the apoptosis pathways, the interaction between apoptosis and OA, the key regulatory factors of chondrocyte apoptosis, and analyzes current drug interventions targeting apoptosis in both preclinical and clinical studies. It also discusses the challenges in treating OA and outlines future research directions to guide upcoming studies. |
| format | Article |
| id | doaj-art-56cd548bcf234705adc0fd17c6d8774d |
| institution | Kabale University |
| issn | 2296-634X |
| language | English |
| publishDate | 2025-03-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cell and Developmental Biology |
| spelling | doaj-art-56cd548bcf234705adc0fd17c6d8774d2025-08-20T03:42:02ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2025-03-011310.3389/fcell.2025.15714481571448Regulation of apoptosis and interaction with cartilage degeneration in osteoarthritisJiahua Mei0Niqin Xiao1Yujiang Xi2Xin Chen3Xuezhi Zha4Lili Cui5Fei Yan6Rui Xue7Yongsen Wang8Yunshu Ma9Yunshu Ma10Yunshu Ma11Yunnan University of Chinese Medicine, Kunming, ChinaYunnan University of Chinese Medicine, Kunming, ChinaYunnan University of Chinese Medicine, Kunming, ChinaYunnan University of Chinese Medicine, Kunming, ChinaYunnan University of Chinese Medicine, Kunming, ChinaYunnan University of Chinese Medicine, Kunming, ChinaYunnan University of Chinese Medicine, Kunming, ChinaYunnan University of Chinese Medicine, Kunming, ChinaYunnan University of Chinese Medicine, Kunming, ChinaYunnan University of Chinese Medicine, Kunming, ChinaThe Key Laboratory of External Drug Delivery System and Preparation Technology in University of Yunnan Province, Kunming, ChinaYunnan Key Laboratory of Dai and Yi medicines, Kunming, ChinaOsteoarthritis (OA) is a chronic degenerative joint disease, primarily characterized by the degradation of the ECM and cartilage degeneration. Articular cartilage is maintained by chondrocytes, which secrete the ECM, making the stability of these cells crucial for joint function. Research has shown that in the later stages of OA, cartilage cavities form, indicating a decline in chondrocyte function. Chondrocyte death is considered a central feature of cartilage degeneration. Apoptosis, a form of programmed cell death, plays a key role in this process. While controlled apoptosis helps remove damaged chondrocytes and protects the cartilage from injury, excessive apoptosis disrupts the balance of the cartilage microenvironment and accelerates OA progression. Therefore, regulating chondrocyte apoptosis may offer a novel approach for preventing and treating cartilage degeneration. This review examines the apoptosis pathways, the interaction between apoptosis and OA, the key regulatory factors of chondrocyte apoptosis, and analyzes current drug interventions targeting apoptosis in both preclinical and clinical studies. It also discusses the challenges in treating OA and outlines future research directions to guide upcoming studies.https://www.frontiersin.org/articles/10.3389/fcell.2025.1571448/fullosteoarthritisapoptosiscartilage degenerationsignaling pathwaysmolecular mechanisms |
| spellingShingle | Jiahua Mei Niqin Xiao Yujiang Xi Xin Chen Xuezhi Zha Lili Cui Fei Yan Rui Xue Yongsen Wang Yunshu Ma Yunshu Ma Yunshu Ma Regulation of apoptosis and interaction with cartilage degeneration in osteoarthritis Frontiers in Cell and Developmental Biology osteoarthritis apoptosis cartilage degeneration signaling pathways molecular mechanisms |
| title | Regulation of apoptosis and interaction with cartilage degeneration in osteoarthritis |
| title_full | Regulation of apoptosis and interaction with cartilage degeneration in osteoarthritis |
| title_fullStr | Regulation of apoptosis and interaction with cartilage degeneration in osteoarthritis |
| title_full_unstemmed | Regulation of apoptosis and interaction with cartilage degeneration in osteoarthritis |
| title_short | Regulation of apoptosis and interaction with cartilage degeneration in osteoarthritis |
| title_sort | regulation of apoptosis and interaction with cartilage degeneration in osteoarthritis |
| topic | osteoarthritis apoptosis cartilage degeneration signaling pathways molecular mechanisms |
| url | https://www.frontiersin.org/articles/10.3389/fcell.2025.1571448/full |
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