Key result
Nicotinamide riboside reverses the HFpEF phenotype in mice by improving mitochondrial function.
Why the study?
Heart failure with preserved ejection fraction is a mortal clinical syndrome without effective therapies, prompting investigation into metabolic dysregulations in HFpEF myocardium using a novel preclinical model.
Does NAD+ repletion improve mitochondrial function and ameliorate the HFpEF phenotype in a preclinical mouse model?
Population
Preclinical mouse model of HFpEF and cardiac tissue from patients with HFpEF
Comparison
Supplementation with nicotinamide riboside or a direct activator of NAD+ biosynthesis vs unsupplemented HFpEF mice
Design
Preclinical animal and human tissue study
Authors
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NAD+ repletion merits further study in HFpEF models; hypothesis-generating from animal data and leaves clinical translation open.
Does NAD+ repletion improve mitochondrial function and ameliorate the HFpEF phenotype in a preclinical mouse model?
Effect estimate: OCR increase
NAD+ repletion improves mitochondrial function and ameliorates the HFpEF phenotype in a preclinical model, suggesting a potential novel therapeutic approach for HFpEF.
Tong et al. (2021) studied Heart failure with preserved ejection fraction (HFpEF). Nicotinamide riboside (NR) vs. Placebo (untreated HFpEF mice) was evaluated on Improvement in palmitoylcarnitine-mediated oxygen consumption rates (OCR) in isolated mitochondria (OCR increase). Nicotinamide riboside supplementation improved mitochondrial function and reversed the HFpEF phenotype in mice, demonstrated by enhanced palmitoylcarnitine-mediated OCR and ameliorated diastolic dysfunction.
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