Rong Peng
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Rong Peng has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Baizhou Xing
Department of Orthopedics, the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, China
1 shared publication - Biao Wu
Department of Orthopedics, the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, China
1 shared publication - Huading Lu
Department of Orthopedics, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, China
1 shared publication - Jie Shang
Department of Orthopedics, the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, China
1 shared publication - Nan Lin
First Department of Orthopedics, Zhongshan City People’s Hospital, Zhongshan 528400, China
1 shared publication - Ning Jiang
Department of Orthopedics, the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, China
1 shared publication
Latest Publications
- Open Access
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 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.
Open AccessInhibition 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 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.