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Editorial
. 2018 May 22;137(21):2274-2277.
doi: 10.1161/CIRCULATIONAHA.117.032626.

Raising NAD in Heart Failure: Time to Translate?

Affiliations
Editorial

Raising NAD in Heart Failure: Time to Translate?

Matthew A Walker et al. Circulation. .
No abstract available

Keywords: Editorials; NAD; heart failure; nicotinamide riboside.

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Figures

Figure 1
Figure 1
NAD+ biosynthesis, consumption and salvage pathways. The intracellular NAD+ pool consists of both oxidized (NAD+) and reduced (NADH) forms. Electrons derived from substrate catabolism are carried by NADH and used for oxidative phosphorylation and biosynthetic reactions. NAD+ also functions as a co-substrate for sirtuins, ADP-ribose transferases, and cyclic ADP-ribose synthases (CD38). Eukaryotes synthesize NAD+ from the amino acid tryptophan via the de novo pathway or NAD+ can be salvaged from nicotinamide (NAM) and converted into nicotinamide mononucleotide (NMN) by nicotinamide phosphoribosyltransferase (Nampt). NMN can also be generated by the phosphorylation of NR by nicotinamide riboside kinase (Nrk).

Comment on

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