Inhibition of Klf10 Attenuates Oxidative Stress-Induced Senescence of Chondrocytes via Modulating Mitophagy
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 in...
| Published in: | Molecules |
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| Main Authors: | , , , , , , , , |
| Format: | Article |
| Language: | English |
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MDPI AG
2023-01-01
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| Online Access: | https://www.mdpi.com/1420-3049/28/3/924 |
| _version_ | 1851908504429789184 |
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| author | Jie Shang Nan Lin Rong Peng Ning Jiang Biao Wu Baizhou Xing Shiyuan Lin Xianghe Xu Huading Lu |
| author_facet | Jie Shang Nan Lin Rong Peng Ning Jiang Biao Wu Baizhou Xing Shiyuan Lin Xianghe Xu Huading Lu |
| author_sort | Jie Shang |
| collection | DOAJ |
| container_title | Molecules |
| description | 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. |
| format | Article |
| id | doaj-art-87cdada69a3c4b34aa5cfbb27bd6bedd |
| institution | Directory of Open Access Journals |
| issn | 1420-3049 |
| language | English |
| publishDate | 2023-01-01 |
| publisher | MDPI AG |
| record_format | Article |
| spelling | doaj-art-87cdada69a3c4b34aa5cfbb27bd6bedd2025-08-19T22:02:53ZengMDPI AGMolecules1420-30492023-01-0128392410.3390/molecules28030924Inhibition of Klf10 Attenuates Oxidative Stress-Induced Senescence of Chondrocytes via Modulating MitophagyJie Shang0Nan Lin1Rong Peng2Ning Jiang3Biao Wu4Baizhou Xing5Shiyuan Lin6Xianghe Xu7Huading Lu8Department of Orthopedics, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, ChinaFirst Department of Orthopedics, Zhongshan City People’s Hospital, Zhongshan 528400, ChinaDepartment of Orthopedics, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, ChinaDepartment of Orthopedics, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, ChinaDepartment of Orthopedics, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, ChinaDepartment of Orthopedics, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, ChinaDepartment of Orthopedics, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, ChinaDepartment of Orthopedics, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, ChinaDepartment of Orthopedics, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, ChinaOsteoarthritis (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.https://www.mdpi.com/1420-3049/28/3/924osteoarthritisKlf10senescencemitochondriaautophagy |
| spellingShingle | Jie Shang Nan Lin Rong Peng Ning Jiang Biao Wu Baizhou Xing Shiyuan Lin Xianghe Xu Huading Lu Inhibition of Klf10 Attenuates Oxidative Stress-Induced Senescence of Chondrocytes via Modulating Mitophagy osteoarthritis Klf10 senescence mitochondria autophagy |
| title | Inhibition of Klf10 Attenuates Oxidative Stress-Induced Senescence of Chondrocytes via Modulating Mitophagy |
| title_full | Inhibition of Klf10 Attenuates Oxidative Stress-Induced Senescence of Chondrocytes via Modulating Mitophagy |
| title_fullStr | Inhibition of Klf10 Attenuates Oxidative Stress-Induced Senescence of Chondrocytes via Modulating Mitophagy |
| title_full_unstemmed | Inhibition of Klf10 Attenuates Oxidative Stress-Induced Senescence of Chondrocytes via Modulating Mitophagy |
| title_short | Inhibition of Klf10 Attenuates Oxidative Stress-Induced Senescence of Chondrocytes via Modulating Mitophagy |
| title_sort | inhibition of klf10 attenuates oxidative stress induced senescence of chondrocytes via modulating mitophagy |
| topic | osteoarthritis Klf10 senescence mitochondria autophagy |
| url | https://www.mdpi.com/1420-3049/28/3/924 |
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