Diabetes Aggravates Post-ischaemic Renal Fibrosis through Persistent Activation of TGF-β1 and Shh Signalling.

ABSTRACT: Diabetes is a risk factor for acute kidney injury (AKI) and chronic kidney disease (CKD). Diabetic patients are easy to progress to CKD after AKI. Currently, activation of fibrotic signalling including transforming growth factor-β1 (TGF-β1) is recognized as a key mechanism in CKD. Here, we investigated the influence of diabetes on CKD progression after AKI by using a unilateral renal ischaemia-reperfusion injury (IRI) model in diabetic mice. IRI induced extensive tubular injury, fibrosis and lymphocyte recruitment at 3 weeks after IRI, irrespective of diabetes. However, diabetes showed sustained tubular injury and markedly increased fibrosis and lymphocyte recruitment compared with non-diabetes at 5 week after IRI. The mRNAs and proteins related to TGF-β1 and sonic hedgehog (Shh) signallin

SUBMITTER: Kim DJ 

PROVIDER: S-EPMC5711892 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature