Raising NAD in Heart Failure
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It has long been known that cellular NAD levels are a critical regulator of metabolism and bioenergetics. The intracellular NAD pool consists of both oxidized (NAD+) and reduced forms (NADH). NAD+ is the main hydride acceptor in intermediary metabolism. Electrons derived from substrate catabolism are carried by NADH and used for oxidative phosphorylation and biosynthetic reactions. These reduction-oxidation reactions are not only essential for mitochondrial function and cell metabolism but also serve as important modulators of cell signaling.1,2 NAD+ functions as a cosubstrate for sirtuin deacylases, ADP-ribose transferases, and cyclic ADP-ribose synthases that govern posttranslational modification of proteins, DNA repair, and inflammatory responses.
Link to full article: https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.117.032626