KL and glomerulosclerosis: In general, animal model studies have depicted a relatively complete causal chain for us: high glucose environment/insulin resistance → endogenous Klotho down-regulation → oxidative stress, inflammation and abnormal activation of Wnt/β-catenin pathway → podocyte injury, glomerulosclerosis, interstitial fibrosis → DKD progression; the intervention of exogenous Klotho or Klotho derived peptide can block this chain in different links, so as to delay or reverse the effect of DKD.