KL and renal fibrosis: In addition, Klotho, through the modulation of proteins such as the aforementioned UCP1, BCL-2, Wnt/β-catenin, PGC-1 alpha, TFEB, and PPAR-γ, promotes the proper mitochondrial function of vital importance in organs that support high metabolic activity, as is the case of the kidneys, and has protective activity against renal fibrosis induced by activation of the Wnt/β-catenin pathway.