Inhibition of Klf10 Attenuates Oxidative Stress-Induced Senescence of Chondrocytes via Modulating Mitophagy

• Published in: Molecules (Basel, Switzerland) Vol. 28; no. 3; p. 924
• Main Authors: Shang, Jie, Lin, Nan, Peng, Rong, Jiang, Ning, Wu, Biao, Xing, Baizhou, Lin, Shiyuan, Xu, Xianghe, Lu, Huading
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 17.01.2023; MDPI
• Subjects: Aged; Apoptosis; Autophagy; Butyl hydroperoxide; Cartilage; Cartilage diseases; Cartilage, Articular - metabolism; Cellular Senescence - physiology; Chondrocytes; Chondrocytes - pathology; Early Growth Response Transcription Factors - metabolism; Homeostasis; Humans; Investigations; Joint diseases; Klf10; Kruppel-Like Transcription Factors - genetics; Kruppel-Like Transcription Factors - metabolism; Localization; Mitochondria; Mitophagy; Osteoarthritis; Osteoarthritis - drug therapy; Oxidative stress; Oxidative Stress - physiology; Proteins; Reactive Oxygen Species - metabolism; Senescence; Therapeutic targets; Transforming growth factors; Massachusetts; China; Germany; senescence; autophagy; mitochondria; osteoarthritis; Klf10
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules28030924

Osteoarthritis (OA) is the most prevalent degenerative joint disease in the elderly. Accumulation of evidence has suggested that chondrocyte senescence plays a significant role in OA development. Here, we show that Krüppel-like factor 10 (Klf10), also named TGFβ inducible early gene-1 (TIEG1), is involved in the pathology of chondrocyte senescence. Knocking down the Klf10 in chondrocytes attenuated the tert-butyl hydroperoxide (TBHP)-induced senescence, inhibited generation of reactive oxygen species (ROS), and maintained mitochondrial homeostasis by activating mitophagy. These findings suggested that knocking down Klf10 inhibited senescence-related changes in chondrocytes and improved cartilage homeostasis, indicating that Klf10 may be a therapeutic target for protecting cartilage against OA.