Sexually dimorphic effects of SARM1 deletion on cardiac NAD metabolism and function.

Nicotinamide adenine dinucleotide (NAD) decline is repeatedly observed in heart disease and its risk factors. Although strategies promoting NAD synthesis to elevate NAD levels improve cardiac function, whether inhibition of NAD consumption can be therapeutic is less investigated. In this study, we examined the role of sterile-α and TIR motif containing 1 (SARM1) NAD hydrolase in mouse hearts, using global SARM1-knockout mice (KO).

NAD Redox Imbalance in the Heart Exacerbates Diabetic Cardiomyopathy.

Background: Diabetes is a risk factor for heart failure and promotes cardiac dysfunction. Diabetic tissues are associated with nicotinamide adenine dinucleotide (NAD) redox imbalance; however, the hypothesis that NAD redox imbalance causes diabetic cardiomyopathy has not been tested. This investigation used mouse models with altered NAD redox balance to test this hypothesis.