Nicotinamide Riboside Preserves Cardiac Function in a Mouse Model of Dilated Cardiomyopathy.

ABSTRACT:

Background

Myocardial metabolic impairment is a major feature in chronic heart failure. As the major coenzyme in fuel oxidation and oxidative phosphorylation and a substrate for enzymes signaling energy stress and oxidative stress response, nicotinamide adenine dinucleotide (NAD⁺) is emerging as a metabolic target in a number of diseases including heart failure. Little is known on the mechanisms regulating homeostasis of NAD⁺ in the failing heart.

Methods

To explore possible alterations of NAD⁺ homeostasis in the failing heart, we quantified the expression of NAD⁺ biosynthetic enzymes in the human failing heart and in the heart of a mouse model of dilated cardiomyopathy (DCM) triggered by Serum Response Factor transcription factor

SUBMITTER: Diguet N 

PROVIDER: S-EPMC6954688 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature