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. 2015 Nov 2;5:15857. doi: 10.1038/srep15857

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(a) Pressure overload decreases cardiac iNampt expression, but myocardial NAD⁺ concentration and Sirt1 deacetylase activity are unchanged. Up-regulation of monocyte-derived eNampt contributes to preservation of myocardial NAD⁺ levels and functional compensation to pressure overload. (b) Pharmacological inhibition of Nampt by FK866 or depletion of monocytes by CloLip suppresses compensatory up-regulation of monocyte-derived eNampt and disrupts the homeostatic mechanism of myocardial NAD⁺ levels and Sirt1 activity, leading to pressure overload-induced cardiac decompensation. (c) Systemic administration of NMN restores myocardial NAD⁺ levels and Sirt1 activity and prevents FK866- or CloLip-induced cardiac decompensation to pressure overload.