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Study · In vitro (cells) · 2025

10 results

FOXO1-NMNAT3 axis dysregulation promotes doxorubicin cardiotoxicity: NAD+ replenishment as a redox-targeted antioxidant therapy.

Cheng F, Zhao M, Wang Q, Xiong H, Yu K, Chen C, Zhu Y, Chen Y, Li J

Redox report : communications in free radical research29 Sept 2025Cited by 4 (Europe PMC)

PMID41021886 (opens in a new tab)PMCIDPMC12481541 (opens in a new tab)DOI10.1080/13510002.2025.2565033 (opens in a new tab)PepBankPUB-41021886
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: CC BY-NC. Results still quote short attributed sentences.

Results from this study10

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In cardiomyocytes, exogenous NAD mitigated doxorubicin-induced cell death.

    In plain wordsIn cells, NAD reduced doxorubicin-induced heart cell death.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseCardiomyocyte death
    Study

    n: not reported in source

    Doxorubicin-exposed cardiomyocytes
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Exogenous NAD+ supplementation mitigated the DOX-induced cardiomyocyte death and redox imbalance.
    1 context sentence
    Summary · context
    Human cardiomyocytes (AC16), mouse atrial myocytes (HL-1), and C57BL/6 mice were used to establish the DIC model.
  2. 02LabIn vitro (cells)Mechanism

    In cardiomyocytes, exogenous NAD mitigated doxorubicin-induced redox imbalance.

    In plain wordsIn cells, NAD reduced doxorubicin-induced redox imbalance.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseRedox imbalance
    Study

    n: not reported in source

    Doxorubicin-exposed cardiomyocytes
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Exogenous NAD+ supplementation mitigated the DOX-induced cardiomyocyte death and redox imbalance.
    1 context sentence
    Summary · context
    Human cardiomyocytes (AC16), mouse atrial myocytes (HL-1), and C57BL/6 mice were used to establish the DIC model.

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. 03AnimalEndogenous levelOther designMechanism

    In integrated DIC models, doxorubicin-induced myocardial oxidative damage accompanied depletion of natural NAD.

    In plain wordsIn integrated mouse and cell models, doxorubicin injury accompanied lower natural NAD levels.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseNAD depletion
    Study

    n: not reported in source

    Integrated in vitro and in vivo DIC models
    Outcome group
    Mitochondrial function · Cardiovascular

    Source sentences

    Summary
    Using integrated in vitro and in vivo models, we demonstrated that DOX induces myocardial oxidative damage accompanied by NAD+ depletion.
    1 context sentence
    Summary · context
    Human cardiomyocytes (AC16), mouse atrial myocytes (HL-1), and C57BL/6 mice were used to establish the DIC model.

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

  2. 04AnimalEndogenous levelOther designMechanism

    In the DIC model, pharmacological CD38 inhibition with 78C failed to restore the natural NAD pool.

    In plain wordsIn integrated models, CD38 inhibition failed to restore natural NAD levels.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    No significant changeNAD restoration with CD38 inhibition
    Study

    n: not reported in source

    Integrated in vitro and in vivo DIC models
    Outcome group
    Mitochondrial function · Cardiovascular

    Source sentences

    Summary
    Mechanistically, pharmacological CD38 inhibition with 78C or genetic silencing failed to restore the NAD+ pool,
    1 context sentence
    Summary · context
    Human cardiomyocytes (AC16), mouse atrial myocytes (HL-1), and C57BL/6 mice were used to establish the DIC model.

    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 alone6

In this study, the peptide 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 the peptide.

  1. 05AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism

    In the DIC model, CD38 genetic silencing failed to restore the NAD pool.

    In plain wordsIn integrated models, CD38 gene silencing failed to restore NAD levels.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    No significant changeNAD restoration with genetic silencing
    Study

    n: not reported in source

    Integrated in vitro and in vivo DIC models
    Outcome group
    Mitochondrial function · Cardiovascular

    Source sentences

    Summary
    Mechanistically, pharmacological CD38 inhibition with 78C or genetic silencing failed to restore the NAD+ pool,
    1 context sentence
    Summary · context
    Human cardiomyocytes (AC16), mouse atrial myocytes (HL-1), and C57BL/6 mice were used to establish the DIC model.

    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. 06AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism

    In the DIC model, NMNAT3 overexpression with NMN administration rescued NAD levels.

    In plain wordsIn integrated models, NMNAT3 overexpression with NMN restored NAD levels.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseNAD rescue with NMNAT3 overexpression and NMN
    Study

    n: not reported in source

    Integrated in vitro and in vivo DIC models
    Outcome group
    Mitochondrial function · Cardiovascular

    Source sentences

    Summary
    whereas nicotinamide mononucleotide adenylyltransferase 3 (NMNAT3) overexpression, combined with nicotinamide mononucleotide (NMN) administration, effectively rescued NAD+ levels and attenuated oxidative stress.
    1 context sentence
    Summary · context
    Human cardiomyocytes (AC16), mouse atrial myocytes (HL-1), and C57BL/6 mice were used to establish the DIC model.

    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. 07AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism

    In the DIC model, NMNAT3 overexpression with NMN administration attenuated oxidative stress while rescuing NAD levels.

    In plain wordsIn integrated models, NMNAT3 overexpression with NMN reduced oxidative stress while restoring NAD levels.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseOxidative stress with NMNAT3 overexpression and NMN
    Study

    n: not reported in source

    Integrated in vitro and in vivo DIC models
    Outcome group
    Mitochondrial function · Cardiovascular

    Source sentences

    Summary
    whereas nicotinamide mononucleotide adenylyltransferase 3 (NMNAT3) overexpression, combined with nicotinamide mononucleotide (NMN) administration, effectively rescued NAD+ levels and attenuated oxidative stress.
    1 context sentence
    Summary · context
    Human cardiomyocytes (AC16), mouse atrial myocytes (HL-1), and C57BL/6 mice were used to establish the DIC model.

    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. 08AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism

    In computational and functional DIC analyses, FOXO1 repressed transcription of the NAD-metabolism enzyme NMNAT3 after doxorubicin exposure.

    In plain wordsIn computational and functional disease-model analyses, FOXO1 repressed the NAD-metabolism enzyme NMNAT3 after doxorubicin exposure.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseFOXO1 repression of NMNAT3
    Study

    n: not reported in source

    Computational and functional DIC analyses
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Computational and functional analyses identified FOXO1 as a transcriptional repressor of NMNAT3 following DOX exposure.
    2 context sentences
    Summary · context
    This study investigated NAD+ metabolism dysregulation as a redox-sensitive mechanism in DIC pathogenesis.
    Summary · context
    Human cardiomyocytes (AC16), mouse atrial myocytes (HL-1), and C57BL/6 mice were used to establish the DIC model.

    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).

  5. 09AnimalNot a test of NMN (nicotinamide mononucleotide) aloneOther designMechanism

    In doxorubicin cardiotoxicity models, NMNAT3 overexpression combined with NMN rescued NAD+ levels.

    In plain wordsIn cardiotoxicity models, NMNAT3 overexpression combined with NMN restored NAD+ levels.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseNAD+ levels
    Study

    n: not reported in source

    Integrated in vitro and in vivo doxorubicin cardiotoxicity models
    Outcome group
    Mitochondrial function · Cardiovascular

    Source sentences

    Summary
    whereas nicotinamide mononucleotide adenylyltransferase 3 (NMNAT3) overexpression, combined with nicotinamide mononucleotide (NMN) administration, effectively rescued NAD+ levels and attenuated oxidative stress.
    2 context sentences
    Summary · context
    Using integrated in vitro and in vivo models, we demonstrated that DOX induces myocardial oxidative damage accompanied by NAD+ depletion.
    Summary · context
    Human cardiomyocytes (AC16), mouse atrial myocytes (HL-1), and C57BL/6 mice were used to establish the DIC model.

    In this study, NMN (nicotinamide mononucleotide) 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 NMN (nicotinamide mononucleotide).

  6. 10AnimalNot a test of NMN (nicotinamide mononucleotide) aloneOther designMechanism

    In doxorubicin cardiotoxicity models, NMNAT3 overexpression combined with NMN attenuated oxidative stress.

    In plain wordsIn cardiotoxicity models, NMNAT3 overexpression combined with NMN reduced oxidative stress.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseOxidative stress
    Study

    n: not reported in source

    Integrated in vitro and in vivo doxorubicin cardiotoxicity models
    Outcome group
    Mitochondrial function · Cardiovascular

    Source sentences

    Summary
    whereas nicotinamide mononucleotide adenylyltransferase 3 (NMNAT3) overexpression, combined with nicotinamide mononucleotide (NMN) administration, effectively rescued NAD+ levels and attenuated oxidative stress.
    2 context sentences
    Summary · context
    Using integrated in vitro and in vivo models, we demonstrated that DOX induces myocardial oxidative damage accompanied by NAD+ depletion.
    Summary · context
    Human cardiomyocytes (AC16), mouse atrial myocytes (HL-1), and C57BL/6 mice were used to establish the DIC model.

    In this study, NMN (nicotinamide mononucleotide) 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 NMN (nicotinamide mononucleotide).

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 3Current

    21 Oct 2026, 12:50 UTC

    Study data updated · source update from Europe PMC

  2. Version 2

    14 Oct 2026, 05:02 UTC

    Study results updated

  3. 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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