CRTAC1 derived from senescent FLSs induces chondrocyte mitochondrial dysfunction via modulating NRF2/SIRT3 axis in osteoarthritis progression

. In addition, SIRT3 reduction could promote the acetylation of FOXO3a and result in mitochondrial dysfunction, which finally contributes to the degradation of chondrocytes. To conclude, this work revealed the critical role and underlying mechanism of senescent FLSs-derived CRTAC1 in OA progression, which provided a potential strategy for the OA therapy.