Article: Nicotinamide Riboside Restores Mitochondrial Function and Improves Heart Failure with Preserved Ejection Fraction: Preclinical Findings

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Cardiovascular Disease Cardiovascular Health Mitochondrial Health Preclinical

Nicotinamide Riboside Restores Mitochondrial Function and Improves Heart Failure with Preserved Ejection Fraction: Preclinical Findings

Synopsis

Heart Failure with Preserved Ejection Fraction (HFpEF) is a serious heart condition without effective treatments. In a mouse model of HFpEF, researchers found impaired mitochondrial fatty acid oxidation linked to excessive acetylation of key enzymes. This hyperacetylation resulted from low NAD+ levels caused by a faulty NAD+ salvage pathway and reduced sirtuin 3 expression. Similar defects in NAD+ biosynthesis genes were seen in human HFpEF heart tissue. Supplementing mice with NR or activating NAD+ biosynthesis improved mitochondrial function and reduced HFpEF symptoms. These results suggest mitochondrial dysfunction in HFpEF is linked to NAD+ deficiency and that restoring NAD+ is a promising therapy.

Journal

Circulation Research

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