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Mitochondrial quality control dysfunction in osteoarthritis: Mechanisms, therapeutic strategies & future prospects
被引:4
|作者:
Cheung, Chiyuen
[1
]
Tu, Shaoqin
[1
]
Feng, Yi
[1
]
Wan, Chuiming
[1
]
Ai, Hong
[1
]
Chen, Zheng
[1
,2
]
机构:
[1] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Stomatol, 600 Tianhe Rd, Guangzhou, Guangdong, Peoples R China
[2] 600, Tianhe Rd, Guangzhou, Guangdong, Peoples R China
基金:
中国国家自然科学基金;
关键词:
Osteoarthritis;
Mitochondrial dysfunction;
Mitochondrial quality control;
Mitophagy;
Oxidative stress;
TARGETED ANTIOXIDANT MITOQ;
OXIDATIVE STRESS;
TRANSCRIPTION-FACTOR;
DNA TRANSCRIPTION;
KETOGENIC DIET;
ACTIVATION;
CHONDROCYTES;
BIOGENESIS;
CARTILAGE;
CELLS;
D O I:
10.1016/j.archger.2024.105522
中图分类号:
R592 [老年病学];
C [社会科学总论];
学科分类号:
03 ;
0303 ;
100203 ;
摘要:
Osteoarthritis (OA) is a prevalent chronic joint disease characterized by articular cartilage degeneration, pain, and disability. Emerging evidence indicates that mitochondrial quality control dysfunction contributes to OA pathogenesis. Mitochondria are essential organelles to generate cellular energy via oxidative phosphorylation and regulate vital processes. Impaired mitochondria can negatively impact cellular metabolism and result in the generation of harmful reactive oxygen species (ROS). Dysfunction in mitochondrial quality control mechanisms has been increasingly linked to OA onset and progression. This review summarizes current knowledge on the role of mitochondrial quality control disruption in OA, highlighting disturbed mitochondrial dynamics, impaired mitochondrial biogenesis, antioxidant defenses and mitophagy. The review also discusses potential therapeutic strategies targeting mitochondrial Quality Control in OA, offering future perspectives on advancing OA therapeutic strategies.
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页数:12
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