Key result
Genetic disruption of Nnt protected mice against both cardiac and metabolic consequences of HFD+L-NAME, preventing increases in E/e' ratio and diastolic stiffness.
Why the study?
Although myocardial redox perturbations accompany HFpEF, the specific role of mitochondrial oxidative stress had not been demonstrated.
Does genetic loss of NNT prevent cardiometabolic alterations and heart failure with preserved ejection fraction in a murine model?
Population
12-week-old male and female Nnt +/+ and Nnt -/- mice (n = 6-10)
Comparison
Nnt -/- vs Nnt +/+ challenged with HFD+L-NAME
Design
Multi-cohort murine study
Follow-up
9 weeks
Authors
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Mitochondrial oxidative stress may drive diastolic dysfunction in cardiometabolic HFpEF models; leaves open whether redox-targeted therapies will benefit patients.
Does genetic loss of NNT prevent cardiometabolic alterations and heart failure with preserved ejection fraction in a murine model?
Absolute Event Rate: 21.5% vs 42.8%
p-value: p=<0.001
Genetic disruption of Nnt protects against the cardiac and metabolic consequences of a high-fat and L-NAME diet in male mice, highlighting a potential novel therapeutic target for HFpEF.
Pepin et al. (2023) studied Heart failure with preserved ejection fraction (HFpEF). Genetic loss of Nicotinamide Nucleotide Transhydrogenase (Nnt-/-) vs. Wild-type NNT (Nnt+/+) was evaluated on E/e' ratio (diastolic dysfunction) (p=<0.001). Genetic disruption of Nnt protected mice against both cardiac and metabolic consequences of HFD+L-NAME, preventing increases in E/e' ratio and diastolic stiffness.
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