Protective Effect of SIRT1 on TGF-β1 Pathway via mTOR in Diabetic Nephropathy

Increasing amounts of evidence show that silent information regulator 2 homolog 1 (SIRT1) expression in mitochondria plays a crucial role in the pathogenesis and development diabetic nephropathy (DN). However, no studies were carried out to evaluate regulation of SIRT1 in TGF-β1/Smad3 deacetylation. In this study, we demonstrated that overexpressing of SIRT1 may decrease TGF-β1 and Smad3 expression in HEK293 cells through regulating mTOR. In addition, the result is the opposite when SIRT1 reduced in HEK293 cells. Taken together, these results demonstrate that although the relationship between SIRT1 and TGF-β1/Smad3 deacetylation has not been reported, and it can be speculated that SIRT1 is closely related to TGF-β1/Smad3 pathway and this situation correlates with the regulation of mTOR and ROS generation. The available evidence implies that SIRT1 has great potential as a clinical target for the prevention and treatment of renal fibrosis in the development of DN.