Fibroblast growth factor 21 (FGF21) alleviates senescence, apoptosis, and extracellular matrix degradation in osteoarthritis via the SIRT1-mTOR signaling pathway

• DOI: 10.1038/s41419-021-04157-x
• Publication Date: 2021-09-23T11:22:17Z
• Authors: Hongwei Lu; Chao Jia; Dengying Wu; Haidong Jin; Zeng Lin; Jun Pan; Xiucui Li; Wei Wang
• Keywords: FGF21; Senescence; Catabolism

Abstract Osteoarthritis (OA) is a complex condition that involves both apoptosis and senescence currently cannot be cured. Fibroblast growth factor 21 (FGF21), known for its role as potent regulator of glucose energy metabolism, protects from various diseases, possibly by mediating autophagy. In the present study, FGF21 in progression OA was investigated vitro vivo experiments. vitro, results revealed administration alleviated apoptosis, senescence, extracellular matrix (ECM) catabolism chondrocytes induced tert-butyl hydroperoxide (TBHP) autophagy flux. Furthermore, CQ, an flux inhibitor, could reverse protective effect FGF21. It observed FGF21-induced enhancement mediated nuclear translocation TFEB, which occurs due to activation SIRT1-mTOR signaling pathway. The experiments demonstrated treatment reduce DMM model. Taken together, these findings suggest ECM via upregulation also reduces development vivo, demonstrating potential therapeutic agent OA.