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Diabetes Aggravates Post-ischaemic Renal Fibrosis through Persistent Activation of TGF-?1 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-?1 (TGF-?1) 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-?1 and sonic hedgehog (Shh) signalling were significantly higher in diabetic versus non-diabetic IRI kidneys. During the in vitro study, the hyperglycaemia induced the activation of TGF-?1 and Shh signalling and also increased profibrogenic phenotype change. However, hyperglycaemic control with insulin did not improve the progression of renal fibrosis and the activation of TGF-?1 and Shh signalling. In conclusion, diabetes promotes CKD progression of AKI via activation of the TGF-?1 and Shh signalling pathways, but insulin treatment was not enough for preventing the progression of renal fibrosis.

SUBMITTER: Kim DJ 

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

REPOSITORIES: biostudies-other

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Diabetes Aggravates Post-ischaemic Renal Fibrosis through Persistent Activation of TGF-β<sub>1</sub> and Shh Signalling.

Kim Dong-Jin DJ   Kang Jun Mo JM   Park Seon Hwa SH   Kwon Hyuk-Kwon HK   Song Seok-Jong SJ   Moon Haena H   Kim Su-Mi SM   Seo Jung-Woo JW   Lee Yu Ho YH   Kim Yang Gyun YG   Moon Ju-Young JY   Lee So-Young SY   Son Youngsook Y   Lee Sang-Ho SH  

Scientific reports 20171201 1


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-β<sub>1</sub> (TGF-β<sub>1</sub>) 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 in  ...[more]

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