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Study · Animal study (in vivo) · mouse · 2017

6 results

Short-term administration of Nicotinamide Mononucleotide preserves cardiac mitochondrial homeostasis and prevents heart failure.

Zhang R, Shen Y, Zhou L, Sangwung P, Fujioka H, Zhang L, Liao X

Journal of molecular and cellular cardiology5 Sept 2017Cited by 62 (Europe PMC)

PMID28882480 (opens in a new tab)PMCIDPMC6257991 (opens in a new tab)DOI10.1016/j.yjmcc.2017.09.001 (opens in a new tab)PepBankPUB-28882480
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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: Publisher copyright. Results still quote short attributed sentences.

Results from this study6

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In KLF4-deficient mice, short-term NMN administration protected against pressure overload-induced heart failure.

    In plain wordsIn mice lacking cardiac KLF4, NMN protected against heart failure caused by pressure overload.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreasePressure overload-induced heart failure
    Study

    mousen: not reported in source

    cardiac-specific KLF4-deficient mice
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Further, we demonstrated that short-term administration of Nicotinamide Mononucleotide (NMN) successfully protected the mutant mice from pressure overload-induced heart failure.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In KLF4-deficient mouse hearts, NMN preserved mitochondrial ultrastructure.

    In plain wordsIn mice lacking cardiac KLF4, NMN preserved mitochondrial structure in the heart.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    Not applicableMitochondrial ultrastructure
    Study

    mousen: not reported in source

    cardiac-specific KLF4-deficient mice
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanically, we showed that NMN preserved mitochondrial ultrastructure, reduced ROS and prevented cell death in the heart.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In KLF4-deficient mouse hearts, NMN reduced ROS.

    In plain wordsIn mice lacking cardiac KLF4, NMN reduced reactive oxygen species in the heart.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseCardiac ROS
    Study

    mousen: not reported in source

    cardiac-specific KLF4-deficient mice
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanically, we showed that NMN preserved mitochondrial ultrastructure, reduced ROS and prevented cell death in the heart.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In KLF4-deficient mouse hearts, NMN prevented cell death.

    In plain wordsIn mice lacking cardiac KLF4, NMN prevented cell death in the heart.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseCardiac cell death
    Study

    mousen: not reported in source

    cardiac-specific KLF4-deficient mice
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanically, we showed that NMN preserved mitochondrial ultrastructure, reduced ROS and prevented cell death in the heart.
  5. 05LabIn vitro (cells)Mechanism

    In cultured cardiomyocytes, NMN significantly increased long-chain fatty acid oxidation.

    In plain wordsIn cells, NMN increased long-chain fatty acid oxidation in cultured heart muscle cells.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseLong-chain fatty acid oxidation
    Study

    n: not reported in source

    cultured cardiomyocytes
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In cultured cardiomyocytes, NMN treatment significantly increased long-chain fatty acid oxidation despite no direct effect on pyruvate oxidation.
  6. 06LabIn vitro (cells)Mechanism

    In cultured cardiomyocytes, NMN had no direct effect on pyruvate oxidation.

    In plain wordsIn cells, NMN had no direct effect on pyruvate oxidation in cultured heart muscle cells.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    No significant changePyruvate oxidation
    Study

    n: not reported in source

    cultured cardiomyocytes
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In cultured cardiomyocytes, NMN treatment significantly increased long-chain fatty acid oxidation despite no direct effect on pyruvate oxidation.

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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