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...

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Published in:Molecules
Main Authors: Jie Shang, Nan Lin, Rong Peng, Ning Jiang, Biao Wu, Baizhou Xing, Shiyuan Lin, Xianghe Xu, Huading Lu
Format: Article
Language:English
Published: MDPI AG 2023-01-01
Subjects:
Online Access:https://www.mdpi.com/1420-3049/28/3/924
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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.
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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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