DPP4 and renal fibrosis: From a mechanistic standpoint, they observed that ACEis protected against renal fibrosis by increasing endogenous levels of anti-fibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP), a substrate of ACE, either by suppressing DPP-4-associated mesenchymal transformation or by elevating the gene expression of antifibrotic miR-29 [63].