Studies involving Sirt1 knockout or overexpression, rescue experiments with p53 3 KR (K117R/K161R/K162R) mutants, ferroptosis inhibitor Lip-1 treatment, and Sirt1-specific agonist SRT1720 administration in animal models consistently support a mechanism in which Sirt1 promotes ferroptosis through p53 deacetylation, thereby mediating CaOx crystal-induced renal fibrosis. This evidence concerns the gene TP53 and renal fibrosis.