Metabolic reprogramming by <i>N</i>‐acetyl‐seryl‐aspartyl‐lysyl‐proline protects against diabetic kidney disease

Abstract

The study envisages that AcSDKP is the endogenous antifibrotic mediator that controls the metabolic switch between glucose and fatty acid metabolism and that suppression of AcSDKP leads to disruption of kidney cell metabolism and activates mesenchymal transformations leading to severe fibrosis in the diabetic kidney.