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Study · Animal study (in vivo) · mouse · 2015

5 results

Monocyte-derived extracellular Nampt-dependent biosynthesis of NAD(+) protects the heart against pressure overload.

Yano M, Akazawa H, Oka T, Yabumoto C, Kudo-Sakamoto Y, Kamo T, Shimizu Y, Yagi H, Naito AT, Lee JK, Suzuki J, Sakata Y, Komuro I

Scientific reports2 Nov 2015Cited by 29 (Europe PMC)

PMID26522369 (opens in a new tab)PMCIDPMC4629142 (opens in a new tab)DOI10.1038/srep15857 (opens in a new tab)PepBankPUB-26522369
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Summary

Nicotinamide phosphoribosyltransferase (Nampt) catalyzes the rate-limiting step in the salvage pathway for nicotinamide adenine dinucleotide (NAD(+)) biosynthesis, and thereby regulates the deacetylase activity of sirtuins. Here we show accommodative regulation of myocardial NAD(+) by monocyte-derived extracellular Nampt (eNampt), which is essential for hemodynamic compensation to pressure overload. Although intracellular Nampt (iNampt) expression was decreased in pressure-overloaded hearts, myocardial NAD(+) concentration and Sirt1 activity were preserved. In contrast, iNampt was up-regulated in spleen and monocytes, and circulating eNampt protein and nicotinamide mononucleotide (NMN), a key precursor of NAD(+), were significantly increased. Pharmacological inhibition of Nampt by FK866 or depletion of monocytes/macrophages by clodronate liposomes disrupted the homeostatic mechanism of myocardial NAD(+) levels and NAD(+)-dependent Sirt1 activity, leading to susceptibility to cardiomyocyte apoptosis and cardiac decompensation in pressure-overloaded mice. These biochemical and hemodynamic defects were prevented by systemic administration of NMN. Our studies uncover a crucial role of monocyte-derived eNampt in myocardial adaptation to pressure overload, and highlight a potential intervention controlling myocardial NAD(+) against heart failure.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study5

4 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Mechanism

    In pressure-overloaded mice, systemic NMN prevented myocardial NAD disruption caused by Nampt inhibition or monocyte/macrophage depletion.

    In plain wordsIn mice with pressure overload, NMN prevented heart NAD disruption caused by Nampt inhibition or immune cell depletion.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    Not applicableMyocardial NAD homeostasis
    Study

    mousen: not reported in source

    pressure-overloaded mice
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated · systemicAs given in this study (mouse).

    Source sentences

    Summary
    These biochemical and hemodynamic defects were prevented by systemic administration of NMN.
    1 context sentence
    Summary · context
    Pharmacological inhibition of Nampt by FK866 or depletion of monocytes/macrophages by clodronate liposomes disrupted the homeostatic mechanism of myocardial NAD(+) levels and NAD(+)-dependent Sirt1 activity,
  2. 02AnimalAnimal study (in vivo)Mechanism

    In pressure-overloaded mice, systemic NMN prevented Sirt1 activity disruption caused by Nampt inhibition or monocyte/macrophage depletion.

    In plain wordsIn mice with pressure overload, NMN prevented Sirt1 disruption caused by Nampt inhibition or immune cell depletion.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    Not applicableNAD-dependent Sirt1 activity
    Study

    mousen: not reported in source

    pressure-overloaded mice
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated · systemicAs given in this study (mouse).

    Source sentences

    Summary
    These biochemical and hemodynamic defects were prevented by systemic administration of NMN.
    1 context sentence
    Summary · context
    Pharmacological inhibition of Nampt by FK866 or depletion of monocytes/macrophages by clodronate liposomes disrupted the homeostatic mechanism of myocardial NAD(+) levels and NAD(+)-dependent Sirt1 activity,
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In pressure-overloaded mice, systemic NMN prevented apoptosis susceptibility induced by Nampt inhibition or monocyte/macrophage depletion.

    In plain wordsIn mice with pressure overload, NMN prevented heart cell apoptosis susceptibility caused by Nampt inhibition or immune cell depletion.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseCardiomyocyte apoptosis susceptibility
    Study

    mousen: not reported in source

    pressure-overloaded mice
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · systemicAs given in this study (mouse).

    Source sentences

    Summary
    These biochemical and hemodynamic defects were prevented by systemic administration of NMN.
    1 context sentence
    Summary · context
    leading to susceptibility to cardiomyocyte apoptosis and cardiac decompensation in pressure-overloaded mice.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In pressure-overloaded mice, systemic NMN prevented cardiac decompensation induced by Nampt inhibition or monocyte/macrophage depletion.

    In plain wordsIn mice with pressure overload, NMN prevented heart decompensation caused by Nampt inhibition or immune cell depletion.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseCardiac decompensation
    Study

    mousen: not reported in source

    pressure-overloaded mice
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · systemicAs given in this study (mouse).

    Source sentences

    Summary
    These biochemical and hemodynamic defects were prevented by systemic administration of NMN.
    1 context sentence
    Summary · context
    leading to susceptibility to cardiomyocyte apoptosis and cardiac decompensation in pressure-overloaded mice.

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 05AnimalEndogenous levelAnimal study (in vivo)Other

    In pressure-overloaded mice, circulating endogenous NMN significantly increased.

    In plain wordsIn mice with pressure overload, natural NMN levels increased in the circulation.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseCirculating NMN
    Study

    mousen: not reported in source

    pressure-overloaded mice
    Outcome group
    Mitochondrial function · Cardiovascular

    Source sentences

    Summary
    In contrast, iNampt was up-regulated in spleen and monocytes, and circulating eNampt protein and nicotinamide mononucleotide (NMN), a key precursor of NAD(+), were significantly increased.
    1 context sentence
    Summary · context
    Although intracellular Nampt (iNampt) expression was decreased in pressure-overloaded hearts, myocardial NAD(+) concentration and Sirt1 activity were preserved.

    This result measures the body's own NMN (nicotinamide mononucleotide). Nobody was given the peptide. It is not evidence about taking it.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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