Sodium-glucose cotransporter 2 inhibitors induce anti-inflammatory and anti-ferroptotic shift in epicardial adipose tissue of subjects with severe heart failure
Authors' conclusion
Our results show decreased inflammation in EAT of patients with severe heart failure treated by SGLT-2i, as compared to patients with heart failure without this therapy. Modulation of EAT inflammatory and metabolic status could represent a novel mechanism behind SGLT-2i-associated cardioprotective effects in patients with heart failure.
Study context
- Population
- Subjects with severe HF with reduced ejection fraction scheduled for heart transplantation or mechanical support implantation; Epicardial adipose tissue (EAT) obtained during surgerymatched
- Participants
- 26 vs 26
- Exposure
- SGLT2i treatment vs no treatment
- SGLT2in = 26
- Without treatmentn = 26reference
- Outcome
- EAT inflammatory and metabolic profile (metabolomic and gene expression analysis)
Methodological detailsmatched for age, BMI and LVEF
- Matched for age, BMI and LVEF
Main finding
As reported in the abstract
- SGLT2i ameliorated inflammation: improved gene expression profile of pro-inflammatory genes in adipose tissue
- Decreased infiltration of immune cells into EAT with SGLT2i
- Enrichment of ether lipids with oleic acid, suggesting reduced disposition to ferroptosis
Observational data: associations, not effects.
Further findings
Matching characteristics · baseline
- Age, years (SGLT2i vs without treatment), n.s.
- 54.0 ± 2.1 vs. 55.3 ± 2.1
- BMI, kg/m² (SGLT2i vs without treatment), n.s.
- 27.8 ± 0.9 vs. 28.8 ± 1.0
- LVEF, % (SGLT2i vs without treatment), n.s.
- 20.7 ± 0.5 vs. 23.2 ± 1.7
Original publication
Sodium-glucose cotransporter 2 inhibitors induce anti-inflammatory and anti-ferroptotic shift in epicardial adipose tissue of subjects with severe heart failure. Cardiovasc Diabetol. Published 28 June 2024. doi:10. 1186/ s12933-024-02298-9
Composed by AI from the published abstract and checked against it. How Briefs are made →