We are analyzing https://link.springer.com/article/10.1007/s10557-023-07517-1.

Title:
Effects of Dapagliflozin on Myocardial Gene Expression in BTBR Mice with Type 2 Diabetes | Cardiovascular Drugs and Therapy
Description:
Background Dapagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor, is approved for the treatment of type 2 diabetes, heart failure, and chronic kidney disease. DAPA-HF and DELIVER trial results demonstrate that the cardiovascular protective effect of dapagliflozin extends to non-diabetic patients. Hence, the mechanism-of-action may extend beyond glucose-lowering and is not completely elucidated. We have previously shown that dapagliflozin reduces cardiac hypertrophy, inflammation, fibrosis, and apoptosis and increases ejection fraction in BTBR mice with type 2 diabetes. Methods We conducted a follow-up RNA-sequencing study on the heart tissue of these animals and performed differential expression and Ingenuity Pathway analysis. Selected markers were confirmed by RT-PCR and Western blot. Results SGLT2 had negligible expression in heart tissue. Dapagliflozin improved cardiac metabolism by decreasing glycolysis and pyruvate utilization enzymes, induced antioxidant enzymes, and decreased expression of hypoxia markers. Expression of inflammation, apoptosis, and hypertrophy pathways was decreased. These observations corresponded to the effects of dapagliflozin in the clinical trials.
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Topics {✒️}

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Questions {❓}

Cardiovascular outcomes trials in type 2 diabetes: where do we go from here?
Effects of SGLT2 inhibition in human kidney proximal tubular cells--renoprotection in diabetic nephropathy?
Is the placental proteome impaired in well-controlled gestational diabetes?

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