SIRT2-mediated FUBP1 Deacetylation Promotes Fibrosis in Diabetic Nephropathy via Activation of the c-Myc Pathway

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SIRT2-mediated FUBP1 Deacetylation Promotes Fibrosis in Diabetic Nephropathy via Activation of the c-Myc Pathway

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Co-author 1

Dan Li lidancl0820@163.com The Third Xiangya Hospital, Central South University Department of Nephrology changsha China -

Co-author 2

zhijun huang huangzj@csu.edu.cn The Third Xiangya Hospital, Central South University Department of Nephrology changsha China -

Co-author 3

Bin Yi yibin2008@csu.edu.cn The Third Xiangya Hospital, Central South University Department of Nephrology changsha China *

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Introduction

The progression of diabetic nephropathy (DN) to end-stage renal disease is primarily driven by renal fibrosis, yet effective therapeutic strategies to prevent this process are limited. Our previous work demonstrated SIRT2 is closely associated with eGFR and tubular injury. However, its specific role and mechanisms in diabetic renal fibrosis remain elusive.

Methods

We employed acetylomics, proteomic mass spectrometry, point mutation, genetic knockout, and pharmacological inhibition to define the role of SIRT2 in DN.

Results

The expression of SIRT2 was significantly increased in the renal tissues of patients with DN and diabetic mice, especially in the proximal renal tubules. SIRT2 deletion or AGK2 intervention (both free and nanoparticle-encapsulated) significantly attenuated renal interstitial fibrosis and ameliorated kidney injury in diabetic mice. In vitro, SIRT2 knockdown reduced the production of profibrotic cytokines and attenuated fibroblasts activation, whereas overexpression of SIRT2 exacerbated the progression of fibrosis. Mechanistically, SIRT2 directly deacetylates far upstream element-binding protein 1 (FUBP1) at lysine 425, followed by an increase in c-Myc expression and in the expression of TGF-β and CTGF. In FUBP1-knockdown HK-2 cells, the FUBP1-K425Q (acetylation mimic) mutant rescued the activation of c-Myc and TGF-β under diabetic conditions.

Conclusion

Our study identified SIRT2 as a critical regulator of fibrosis in DN through deacetylation of FUBP1 and activation of the c-Myc pathway.

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