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Study · Animal study (in vivo) · mouse · 2021

3 results

Nicotinamide mononucleotide ameliorates senescence in alveolar epithelial cells.

Fang T, Yang J, Liu L, Xiao H, Wei X

MedComm27 May 2021Cited by 19 (Europe PMC)

Summary

Alveolar epithelial cells (ACEs) gradually senescent as aging, which is one of the main causes of respiratory defense and function decline. Investigating the mechanisms of ACE senescence is important for understanding how the human respiratory system works. NAD+ is reported to reduce during the aging process. Supplementing NAD+ intermediates can activate sirtuin deacylases (SIRT1-SIRT7), which regulates the benefits of exercise and dietary restriction, reduce the level of intracellular oxidative stress, and improve mitochondrial function, thereby reversing cell senescence. We showed that nicotinamide mononucleotide (NMN) could effectively mitigate age-associated physiological decline in the lung of 8-10 months old C57BL/6 mice and bleomycin-induced pulmonary fibrosis in young mice of 6-8 weeks. Besides, the treatment of primary ACEs with NMN can markedly ameliorate cell senescence phenotype in vitro. These findings to improve the respiratory system function and reduce the incidence and mortality from respiratory diseases in the elderly are of great significance.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In aging mice, NMN mitigated age-associated physiological decline in the lung.

    In plain wordsIn mice, NMN reduced age-associated decline in lung physiology.

    Outcome
    DecreaseAge-associated lung decline
    Study

    mousen: not reported in source

    8-10 months old C57BL/6 mice
    Outcome group
    Aging markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We showed that nicotinamide mononucleotide (NMN) could effectively mitigate age-associated physiological decline in the lung of 8-10 months old C57BL/6 mice and bleomycin-induced pulmonary fibrosis in young mice of 6-8 weeks.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In young mice, NMN mitigated bleomycin-induced pulmonary fibrosis.

    In plain wordsIn young mice, NMN reduced lung fibrosis induced by bleomycin.

    Outcome
    DecreasePulmonary fibrosis
    Study

    mousen: not reported in source

    bleomycin-induced pulmonary fibrosis
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We showed that nicotinamide mononucleotide (NMN) could effectively mitigate age-associated physiological decline in the lung of 8-10 months old C57BL/6 mice and bleomycin-induced pulmonary fibrosis in young mice of 6-8 weeks.
  3. 03LabIn vitro (cells)Efficacy outcome

    In primary alveolar epithelial cells, NMN markedly ameliorated the senescence phenotype.

    In plain wordsIn cells, NMN reduced the senescence phenotype in primary alveolar epithelial cells.

    Outcome
    DecreaseCell senescence phenotype
    Study

    n: not reported in source

    primary alveolar epithelial cells
    Outcome group
    Aging markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Besides, the treatment of primary ACEs with NMN can markedly ameliorate cell senescence phenotype in vitro.

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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