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However, SGLT2-i could reduce renal and extra-renal glucotoxicity by inhibiting many pro-inflammatory pathways such as low serum ketone levels, hyperuricemia, oxidative stress and advanced glycation-end products (AGEs) induced by hyperglycemia ( Indeed, there is a growing body of evidence suggesting a significant beneficial class effect associated with SGLT2 inhibition, resulting in MACE, cardiovascular death and hospitalization for heart failure (HHF) reduction, despite some variabilities in the findings provided by individual CVOTs (40)

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