Advances in the study of mitophagy in osteoarthritis
Osteoarthritis (OA), characterized by cartilage degeneration, synovial inflammation, and subchondral bone remodeling, is among the most common musculoskeletal disorders globally in people over 60 years of age. The initiation and progression of OA involves the abnormal metabolism of chondrocytes as an important pathogenic process. Cartilage degeneration features mitochondrial dysfunction as one of the important causative factors of abnormal chondrocyte metabolism. Therefore, maintaining mitochondrial homeostasis is an important strategy to mitigate OA. Mitophagy is a vital process for autophagosomes to target, engulf, and remove damaged and dysfunctional mitochondria, thereby maintaining mitochondrial homeostasis. Cumulative studies have revealed a strong association between mitophagy and OA, suggesting that the regulation of mitophagy may be a novel therapeutic direction for OA. By reviewing the literature on mitophagy and OA published in recent years, this paper elaborates the potential mechanism of mitophagy regulating OA, thus providing a theoretical basis for studies related to mitophagy to develop new treatment options for OA.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:25 |
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| Enthalten in: |
Journal of Zhejiang University. Science. B - 25(2024), 3 vom: 15. März, Seite 197-211 |
| Sprache: |
Englisch |
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| Weiterer Titel: |
线粒体自噬调控骨关节炎的最新进展 |
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| Beteiligte Personen: |
Cao, Hong [VerfasserIn] |
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| Links: |
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| Themen: |
Apoptosis |
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| Anmerkungen: |
Date Completed 11.03.2024 Date Revised 11.03.2024 published: Print Citation Status MEDLINE |
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| doi: |
10.1631/jzus.B2300402 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM369433793 |
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| 245 | 1 | 0 | |a Advances in the study of mitophagy in osteoarthritis |
| 246 | 3 | 3 | |a 线粒体自噬调控骨关节炎的最新进展 |
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| 520 | |a Osteoarthritis (OA), characterized by cartilage degeneration, synovial inflammation, and subchondral bone remodeling, is among the most common musculoskeletal disorders globally in people over 60 years of age. The initiation and progression of OA involves the abnormal metabolism of chondrocytes as an important pathogenic process. Cartilage degeneration features mitochondrial dysfunction as one of the important causative factors of abnormal chondrocyte metabolism. Therefore, maintaining mitochondrial homeostasis is an important strategy to mitigate OA. Mitophagy is a vital process for autophagosomes to target, engulf, and remove damaged and dysfunctional mitochondria, thereby maintaining mitochondrial homeostasis. Cumulative studies have revealed a strong association between mitophagy and OA, suggesting that the regulation of mitophagy may be a novel therapeutic direction for OA. By reviewing the literature on mitophagy and OA published in recent years, this paper elaborates the potential mechanism of mitophagy regulating OA, thus providing a theoretical basis for studies related to mitophagy to develop new treatment options for OA | ||
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| 650 | 4 | |a Chondrocyte | |
| 650 | 4 | |a Mitochondria | |
| 650 | 4 | |a Mitophagy | |
| 650 | 4 | |a Osteoarthritis | |
| 700 | 1 | |a Zhou, Xuchang |e verfasserin |4 aut | |
| 700 | 1 | |a Xu, Bowen |e verfasserin |4 aut | |
| 700 | 1 | |a Hu, Han |e verfasserin |4 aut | |
| 700 | 1 | |a Guo, Jianming |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Miao |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Nan |e verfasserin |4 aut | |
| 700 | 1 | |a Jun, Zou |e verfasserin |4 aut | |
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