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Study · Animal study (in vivo) · mouse · 2024

4 results

Nicotinamide Mononucleotide Supplementation Alleviates Doxorubicin-Induced Multi-Organ Fibrosis.

Wen F, Xu A, Wei W, Yang S, Xi Z, Ge Y, Wu S, Ju Z

International journal of molecular sciences13 May 2024Cited by 5 (Europe PMC)

PMID38791345 (opens in a new tab)PMCIDPMC11120852 (opens in a new tab)DOI10.3390/ijms25105303 (opens in a new tab)PepBankPUB-38791345
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Summary

Doxorubicin (DOX) is a potent chemotherapeutic agent known for its multi-organ toxicity, especially in the heart, which limits its clinical application. The toxic side effects of DOX, including DNA damage, oxidative stress, mitochondrial dysfunction and cell apoptosis, are intricately linked to the involvement of nicotinamide adenine dinucleotide (NAD+). To assess the effectiveness of the NAD+ precursor nicotinamide mononucleotide (NMN) in counteracting the multi-organ toxicity of DOX, a mouse model was established through DOX administration, which led to significant reductions in NAD+ in tissues with evident injury, including the heart, liver and lungs. NMN treatment alleviated both multi-organ fibrosis and mortality in mice. Mechanistically, tissue fibrosis, macrophage infiltration and DOX-related cellular damage, which are potentially implicated in the development of multi-organ fibrosis, could be attenuated by NAD+ restoration. Our findings provide compelling evidence for the benefits of NMN supplementation in mitigating the adverse effects of chemotherapeutic drugs on multiple organs.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study4

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice with doxorubicin injury, NMN alleviated multi-organ fibrosis.

    In plain wordsIn mice, NMN reduced scarring across organs after doxorubicin exposure.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseMulti-organ fibrosis
    Study

    mousen: not reported in source

    doxorubicin-induced injury
    Outcome group
    Lung injury and fibrosis · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN treatment alleviated both multi-organ fibrosis and mortality in mice.
    1 context sentence
    Summary · context
    To assess the effectiveness of the NAD+ precursor nicotinamide mononucleotide (NMN) in counteracting the multi-organ toxicity of DOX, a mouse model was established through DOX administration, which led to significant reductions in NAD+ in tissues with evident injury, including the heart, liver and lungs.
  2. 02AnimalAnimal study (in vivo)Safety outcome

    In mice with doxorubicin injury, NMN reduced mortality.

    In plain wordsIn mice, NMN reduced deaths after doxorubicin exposure.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseMortality
    Study

    mousen: not reported in source

    doxorubicin-induced injury
    Outcome group
    Mortality · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN treatment alleviated both multi-organ fibrosis and mortality in mice.
    1 context sentence
    Summary · context
    To assess the effectiveness of the NAD+ precursor nicotinamide mononucleotide (NMN) in counteracting the multi-organ toxicity of DOX, a mouse model was established through DOX administration, which led to significant reductions in NAD+ in tissues with evident injury, including the heart, liver and lungs.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In mice with doxorubicin injury, NAD restoration associated with NMN could attenuate macrophage infiltration.

    In plain wordsIn mice, NAD restoration associated with NMN could reduce macrophage infiltration after doxorubicin exposure.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseMacrophage infiltration
    Study

    mousen: not reported in source

    doxorubicin-induced injury
    Outcome group
    Inflammation markers · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, tissue fibrosis, macrophage infiltration and DOX-related cellular damage, which are potentially implicated in the development of multi-organ fibrosis, could be attenuated by NAD+ restoration.
    1 context sentence
    Summary · context
    To assess the effectiveness of the NAD+ precursor nicotinamide mononucleotide (NMN) in counteracting the multi-organ toxicity of DOX, a mouse model was established through DOX administration, which led to significant reductions in NAD+ in tissues with evident injury, including the heart, liver and lungs.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In mice with doxorubicin injury, NAD restoration associated with NMN could attenuate cellular damage.

    In plain wordsIn mice, NAD restoration associated with NMN could reduce cell damage after doxorubicin exposure.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseCellular damage
    Study

    mousen: not reported in source

    doxorubicin-induced injury
    Outcome group
    Cell viability and death · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, tissue fibrosis, macrophage infiltration and DOX-related cellular damage, which are potentially implicated in the development of multi-organ fibrosis, could be attenuated by NAD+ restoration.
    1 context sentence
    Summary · context
    To assess the effectiveness of the NAD+ precursor nicotinamide mononucleotide (NMN) in counteracting the multi-organ toxicity of DOX, a mouse model was established through DOX administration, which led to significant reductions in NAD+ in tissues with evident injury, including the heart, liver and lungs.

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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