SIRT3 and renal fibrosis: Our data revealed that Sirt3 was required for PAA to attenuate renal fibroblast activation and interstitial fibrosis, and firstly demonstrated that Sirt3 deacetylated β-catenin mainly at K49 site thus suppressing β-catenin stability and following pro-fibrotic downstream target gene expressions, highlighting Sirt3 functioned as a promising therapeutic target of renal fibrosis.