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Study · Animal study (in vivo) · 2010

13 results

Exogenous NAD blocks cardiac hypertrophic response via activation of the SIRT3-LKB1-AMP-activated kinase pathway.

Pillai VB, Sundaresan NR, Kim G, Gupta M, Rajamohan SB, Pillai JB, Samant S, Ravindra PV, Isbatan A, Gupta MP

The Journal of biological chemistry24 Nov 2009Cited by 340 (Europe PMC)

PMID19940131 (opens in a new tab)PMCIDPMC2823454 (opens in a new tab)DOI10.1074/jbc.m109.077271 (opens in a new tab)PepBankPUB-19940131
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Summary

Since the discovery of NAD-dependent deacetylases, sirtuins, it has been recognized that maintaining intracellular levels of NAD is crucial for the management of stress response of cells. Here we show that agonist-induced cardiac hypertrophy is associated with loss of intracellular levels of NAD, but not exercise-induced physiologic hypertrophy. Exogenous addition of NAD was capable of maintaining intracellular levels of NAD and blocking the agonist-induced cardiac hypertrophic response in vitro as well as in vivo. NAD treatment blocked the activation of pro-hypertrophic Akt1 signaling, and augmented the activity of anti-hypertrophic LKB1-AMPK signaling in the heart, which prevented subsequent induction of mTOR-mediated protein synthesis. By using gene knock-out and transgenic mouse models of SIRT3 and SIRT1, we showed that the anti-hypertrophic effects of exogenous NAD are mediated through activation of SIRT3, but not SIRT1. SIRT3 deacetylates and activates LKB1, thus augmenting the activity of the LKB1-AMPK pathway. These results reveal a novel role of NAD as an inhibitor of cardiac hypertrophic signaling, and suggest that prevention of NAD depletion may be critical in the treatment of cardiac hypertrophy and heart failure.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study13

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In vivo, exogenous NAD maintained intracellular NAD levels during agonist-induced cardiac hypertrophy.

    In plain wordsIn animals, exogenous NAD maintained intracellular NAD levels during agonist-induced cardiac hypertrophy.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseIntracellular NAD maintenance in vivo
    Study

    n: not reported in source

    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Exogenous addition of NAD was capable of maintaining intracellular levels of NAD and blocking the agonist-induced cardiac hypertrophic response in vitro as well as in vivo.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In vivo, exogenous NAD blocked agonist-induced cardiac hypertrophy.

    In plain wordsIn animals, exogenous NAD blocked agonist-induced cardiac hypertrophy.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseCardiac hypertrophy in vivo
    Study

    n: not reported in source

    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Exogenous addition of NAD was capable of maintaining intracellular levels of NAD and blocking the agonist-induced cardiac hypertrophic response in vitro as well as in vivo.
  3. 03AnimalOther designMechanism

    In the heart, NAD blocked activation of pro-hypertrophic Akt1 signaling.

    In plain wordsIn animal heart models, NAD blocked activation of pro-hypertrophic Akt1 signaling.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseAkt1 signaling
    Study

    n: not reported in source

    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NAD treatment blocked the activation of pro-hypertrophic Akt1 signaling, and augmented the activity of anti-hypertrophic LKB1-AMPK signaling in the heart, which prevented subsequent induction of mTOR-mediated protein synthesis.
  4. 04AnimalOther designMechanism

    In the heart, NAD augmented anti-hypertrophic LKB1-AMPK signaling activity.

    In plain wordsIn animal heart models, NAD increased anti-hypertrophic LKB1-AMPK signaling activity.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseLKB1-AMPK signaling
    Study

    n: not reported in source

    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NAD treatment blocked the activation of pro-hypertrophic Akt1 signaling, and augmented the activity of anti-hypertrophic LKB1-AMPK signaling in the heart, which prevented subsequent induction of mTOR-mediated protein synthesis.
  5. 05AnimalOther designMechanism

    In the heart, NAD signaling effects prevented subsequent induction of mTOR-mediated protein synthesis.

    In plain wordsIn animal heart models, NAD prevented subsequent induction of mTOR-mediated protein synthesis.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreasemTOR-mediated protein synthesis
    Study

    n: not reported in source

    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NAD treatment blocked the activation of pro-hypertrophic Akt1 signaling, and augmented the activity of anti-hypertrophic LKB1-AMPK signaling in the heart, which prevented subsequent induction of mTOR-mediated protein synthesis.
  6. 06LabIn vitro (cells)Mechanism

    In vitro, exogenous NAD maintained intracellular NAD levels during agonist-induced cardiac hypertrophy.

    In plain wordsIn lab tests, exogenous NAD maintained intracellular NAD levels during agonist-induced cardiac hypertrophy.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseIntracellular NAD maintenance in vitro
    Study

    n: not reported in source

    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Exogenous addition of NAD was capable of maintaining intracellular levels of NAD and blocking the agonist-induced cardiac hypertrophic response in vitro as well as in vivo.
  7. 07LabIn vitro (cells)Efficacy outcome

    In vitro, exogenous NAD blocked agonist-induced cardiac hypertrophy.

    In plain wordsIn lab tests, exogenous NAD blocked agonist-induced cardiac hypertrophy.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseCardiac hypertrophy in vitro
    Study

    n: not reported in source

    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Exogenous addition of NAD was capable of maintaining intracellular levels of NAD and blocking the agonist-induced cardiac hypertrophic response in vitro as well as in vivo.

Natural levels measured2

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. 08AnimalEndogenous levelOther designMechanism

    In cardiac hypertrophy models, agonist-induced hypertrophy was associated with lower intracellular NAD levels.

    In plain wordsIn animal cardiac hypertrophy models, agonist-induced hypertrophy was linked to lower natural NAD levels.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseNAD in agonist-induced hypertrophy
    Study

    n: not reported in source

    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    Here we show that agonist-induced cardiac hypertrophy is associated with loss of intracellular levels of NAD, but not exercise-induced physiologic hypertrophy.

    This result measures the body's own NAD+ (nicotinamide adenine dinucleotide). Nobody was given the peptide. It is not evidence about taking it.

  2. 09AnimalEndogenous levelOther designMechanism

    In cardiac hypertrophy models, exercise-induced physiological hypertrophy was not associated with loss of intracellular NAD.

    In plain wordsIn animal cardiac hypertrophy models, exercise-induced hypertrophy was not linked to lower natural NAD levels.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    No significant changeNAD in exercise-induced hypertrophy
    Study

    n: not reported in source

    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    Here we show that agonist-induced cardiac hypertrophy is associated with loss of intracellular levels of NAD, but not exercise-induced physiologic hypertrophy.

    This result measures the body's own NAD+ (nicotinamide adenine dinucleotide). Nobody was given the peptide. It is not evidence about taking it.

Studies that did not test the peptide alone4

In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking NAD+ (nicotinamide adenine dinucleotide).

  1. 10AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Mechanism

    In knockout and transgenic mouse models, SIRT3 activation mediated the anti-hypertrophic effects of exogenous NAD.

    In plain wordsIn mice, gene-model experiments showed that SIRT3 activation mediated the anti-hypertrophic effects of exogenous NAD.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    Not applicableSIRT3 mediation of anti-hypertrophic effects
    Study

    mousen: not reported in source

    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    By using gene knock-out and transgenic mouse models of SIRT3 and SIRT1, we showed that the anti-hypertrophic effects of exogenous NAD are mediated through activation of SIRT3, but not SIRT1.

    In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).

  2. 11AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Mechanism

    In knockout and transgenic mouse models, SIRT1 did not mediate the anti-hypertrophic effects of exogenous NAD.

    In plain wordsIn mice, gene-model experiments showed that SIRT1 did not mediate the anti-hypertrophic effects of exogenous NAD.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    No significant changeSIRT1 mediation of anti-hypertrophic effects
    Study

    mousen: not reported in source

    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    By using gene knock-out and transgenic mouse models of SIRT3 and SIRT1, we showed that the anti-hypertrophic effects of exogenous NAD are mediated through activation of SIRT3, but not SIRT1.

    In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).

  3. 12AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Mechanism

    In mouse gene models, SIRT3 deacetylated LKB1.

    In plain wordsIn mice, SIRT3 removed acetyl groups from LKB1.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    Not applicableLKB1 deacetylation
    Study

    mousen: not reported in source

    SIRT3 and SIRT1 knockout and transgenic mouse models
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    SIRT3 deacetylates and activates LKB1, thus augmenting the activity of the LKB1-AMPK pathway.
    1 context sentence
    Summary · context
    By using gene knock-out and transgenic mouse models of SIRT3 and SIRT1, we showed that the anti-hypertrophic effects of exogenous NAD are mediated through activation of SIRT3, but not SIRT1.

    In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).

  4. 13AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Mechanism

    In mouse gene models, SIRT3 activated LKB1.

    In plain wordsIn mice, SIRT3 activated LKB1.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseLKB1 activation
    Study

    mousen: not reported in source

    SIRT3 and SIRT1 knockout and transgenic mouse models
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    SIRT3 deacetylates and activates LKB1, thus augmenting the activity of the LKB1-AMPK pathway.
    1 context sentence
    Summary · context
    By using gene knock-out and transgenic mouse models of SIRT3 and SIRT1, we showed that the anti-hypertrophic effects of exogenous NAD are mediated through activation of SIRT3, but not SIRT1.

    In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).

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

    14 Oct 2026, 05:02 UTC

    Study results updated

  2. Version 1

    14 Oct 2026, 01:46 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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