Combination of genetic eNOS deficiency and high-fat diet induces reproducible cardiometabolic HFpEF.
Heart failure with preserved ejection fraction (HFpEF) is a complex, multi-organ cardiometabolic syndrome lacking universally effective therapies. We developed and validated a robust murine model leveraging complete, constitutive genetic endothelial nitric oxide synthase deficiency (eNOS KO) coupled with metabolic stress via a high-fat diet (HFD) in both male and female cohorts.
Heart failure with preserved ejection fraction (HFpEF) is a complex, multi-organ cardiometabolic syndrome lacking universally effective therapies. We developed and validated a robust murine model leveraging complete, constitutive genetic endothelial nitric oxide synthase deficiency (eNOS KO) coupled with metabolic stress via a high-fat diet (HFD) in both male and female cohorts.
What the study was
- Study design
- Cohort/Observational Study
- Category
- Treatment Innovation
- Maturity
- Validated
- Journal
- Redox Biol
Why it surfaced
Matched watchlist topic 'Cardiovascular-metabolic: GLP-1, SGLT2, cardiometabolic risk'. Study design: Cohort/Observational Study. Score: 8/10 (N:3, R:3, D:1, P:1).
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