Quercetin attenuates tendon stem/progenitor cell senescence and promotes aged tendon repair via AKT/NF-κB/NLRP3-mediated mitophagy activation.

Hao Wang, Yu-Cheng Gao, Guang-Chun Dai, Pan-Pan Lu, Ying-Juan Li, Mu-Min Cao, Xiao-Yu Liu, Ren-Wang Sheng, Liu Shi, Cheng Zhang, Wen-Guo Cui, Yun-Feng Rui

Department of Orthopaedics, Zhongda Hospital, School of Medicine, Southeast University, No. 87 Ding Jia Qiao, Nanjing, Jiangsu 210009, PR China; Orthopaedic Trauma Institute, Southeast University, No. 87 Ding Jia Qiao, Nanjing, Jiangsu 210009, PR China; Trauma Center, Zhongda Hospital, School of Medicine, Southeast University, No. 87 Ding Jia Qiao, Nanjing, Jiangsu 210009, PR China. · pubmed

Paper

Abstract

Aged tendon exhibits impaired regenerative capacity due to the accumulation of senescent tendon stem/progenitor cells (TSPCs), which secrete senescence-associated secretory phenotype (SASP) factors and display compromised differentiation. Despite its clinical significance in recurrent tendon injury, no targeted therapies exist to counteract TSPCs senescence.

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Research summary

Quercetin promotes aged tendon repair by attenuating TSPC senescence through mitophagy activation. This research addresses the underlying mechanisms of cellular senescence, which is a key factor in aging and age-related tissue degeneration.

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