Cardioprotection by nicotinamide mononucleotide (NMN): Involvement of glycolysis and acidic pH.

ABSTRACT: Stimulation of the cytosolic NAD⁺ dependent deacetylase SIRT1 is cardioprotective against ischemia-reperfusion (IR) injury. NAD⁺ precursors including nicotinamide mononucleotide (NMN) are thought to induce cardioprotection via SIRT1. Herein, while NMN protected perfused hearts against IR (functional recovery: NMN 42 ± 7% vs. vehicle 11 ± 3%), this protection was insensitive to the SIRT1 inhibitor splitomicin (recovery 47 ± 8%). Although NMN-induced cardioprotection was absent in Sirt3^-/- hearts (recovery 9 ± 5%), this was likely due to enhanced baseline injury in Sirt3^-/- (recovery 6 ± 2%), since similar injury levels in WT hearts also blunted the protective efficacy of NMN. Considering alternative cardiac effects of NMN, and the requirement of g

SUBMITTER: Nadtochiy SM 

PROVIDER: S-EPMC6103815 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature