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Study · Animal study (in vivo) · mouse · 2023

5 results

Improving lysosomal ferroptosis with NMN administration protects against heart failure.

Yagi M, Do Y, Hirai H, Miki K, Toshima T, Fukahori Y, Setoyama D, Abe C, Nabeshima YI, Kang D, Uchiumi T

Life science alliance4 Oct 2023Cited by 33 (Europe PMC)

PMID37793777 (opens in a new tab)PMCIDPMC10551641 (opens in a new tab)DOI10.26508/lsa.202302116 (opens in a new tab)PepBankPUB-37793777
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Summary

Myocardial mitochondria are primary sites of myocardial energy metabolism. Mitochondrial disorders are associated with various cardiac diseases. We previously showed that mice with cardiomyocyte-specific knockout of the mitochondrial translation factor p32 developed heart failure from dilated cardiomyopathy. Mitochondrial translation defects cause not only mitochondrial dysfunction but also decreased nicotinamide adenine dinucleotide (NAD+) levels, leading to impaired lysosomal acidification and autophagy. In this study, we investigated whether nicotinamide mononucleotide (NMN) administration, which compensates for decreased NAD+ levels, improves heart failure because of mitochondrial dysfunction. NMN administration reduced damaged lysosomes and improved autophagy, thereby reducing heart failure and extending the lifespan in p32cKO mice. We found that lysosomal damage due to mitochondrial dysfunction induced ferroptosis, involving the accumulation of iron in lysosomes and lipid peroxide. The ameliorative effects of NMN supplementation were found to strongly affect lysosomal function rather than mitochondrial function, particularly lysosome-mediated ferroptosis. NMN supplementation can improve lysosomal, rather than mitochondrial, function and prevent chronic heart failure.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study5

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In p32cKO mice, NMN reduced damaged lysosomes.

    In plain wordsIn mice with heart-specific p32 deletion, NMN reduced damaged lysosomes.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseDamaged lysosomes
    Study

    mousen: not reported in source

    cardiomyocyte-specific p32 knockout mice
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN administration reduced damaged lysosomes and improved autophagy, thereby reducing heart failure and extending the lifespan in p32cKO mice.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In p32cKO mice, NMN improved autophagy.

    In plain wordsIn mice with heart-specific p32 deletion, NMN improved autophagy.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseAutophagy
    Study

    mousen: not reported in source

    cardiomyocyte-specific p32 knockout mice
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN administration reduced damaged lysosomes and improved autophagy, thereby reducing heart failure and extending the lifespan in p32cKO mice.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In p32cKO mice, NMN reduced heart failure.

    In plain wordsIn mice with heart-specific p32 deletion, NMN reduced heart failure.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseHeart failure
    Study

    mousen: not reported in source

    cardiomyocyte-specific p32 knockout mice
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN administration reduced damaged lysosomes and improved autophagy, thereby reducing heart failure and extending the lifespan in p32cKO mice.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In p32cKO mice, NMN extended lifespan.

    In plain wordsIn mice with heart-specific p32 deletion, NMN extended lifespan.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseLifespan
    Study

    mousen: not reported in source

    cardiomyocyte-specific p32 knockout mice
    Outcome group
    Mortality · Aging and longevity
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN administration reduced damaged lysosomes and improved autophagy, thereby reducing heart failure and extending the lifespan in p32cKO mice.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In the heart failure model, NMN effects predominantly involved lysosomal function, particularly lysosome-mediated ferroptosis, rather than mitochondrial function.

    In plain wordsIn mice, NMN effects mainly involved lysosomal function and lysosome-mediated ferroptosis rather than mitochondrial function.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    Not applicableLysosomal versus mitochondrial effects
    Study

    mousen: not reported in source

    cardiomyocyte-specific p32 knockout mice
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The ameliorative effects of NMN supplementation were found to strongly affect lysosomal function rather than mitochondrial function, particularly lysosome-mediated ferroptosis.

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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