The effect of Dapagliflozin on diabetic nephropathy through PRMT1-FoxO1 pathway-mediated autophagy

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Dapagliflozin significantly reduced the fasting blood glucose levels of nephropathy mice in the DK group, improved insulin resistance and pathological changes such as thickening of the glomerular basement membrane and fusion of podocyte foot processes, and significantly decreased the renal function indicators of mice. In terms of the molecular mechanism, the expression of PRMT1 in the kidneys of the DK group was upregulated, while the expressions of FoxO1 and its downstream autophagy markers (LC3, Beclin1, ATG12) were downregulated. In the Dap group, the expression of PRMT1 was decreased, the expressions of FoxO1 and its downstream autophagy markers were restored, and the DNA methylation level of FoxO1 was reduced.

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