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Study · Animal study (in vivo) · mouse · 2025

15 results

Nicotinamide mononucleotide protects septic hearts in mice via preventing cyclophilin F modification and lysosomal dysfunction.

Ni R, Ji XY, Cao T, Liu XW, Wang C, Lu C, Peng A, Zhang ZX, Fan GC, Zhang J, Su ZL, Peng TQ

Acta pharmacologica Sinica2 Dec 2024Cited by 14 (Europe PMC)

PMID39623043 (opens in a new tab)PMCIDPMC11950505 (opens in a new tab)DOI10.1038/s41401-024-01424-3 (opens in a new tab)PepBankPUB-39623043
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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 study15

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In septic mouse hearts, NMN attenuated LPS-induced mitochondrial ROS production.

    In plain wordsIn mice with sepsis, NMN reduced LPS-induced mitochondrial reactive oxygen production in hearts.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseMitochondrial ROS
    Study

    mousen: not reported in source

    LPS-induced sepsis
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    500 mg/kg · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    NMN administration attenuated LPS-induced deteriorative effects.
    3 context sentences
    Summary · context
    We showed that LPS treatment markedly increased mitochondrial ROS production and induced lysosomal dysfunction and aberrant autophagy in cardiomyocytes and mouse hearts, leading to inflammatory responses and myocardial injury and dysfunction in septic mice.
    Summary · context
    Sepsis was induced in mice by injection of LPS (4 mg/kg, i.p.).
    Summary · context
    Then mice received NMN (500 mg/kg, i.p.) or mito-TEMPO (0.7 mg/kg, i.p.) right after LPS injection, and subjected to echocardiography for assessing myocardial function.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In septic mouse hearts, NMN attenuated LPS-induced lysosomal dysfunction.

    In plain wordsIn mice with sepsis, NMN reduced LPS-induced lysosomal dysfunction in hearts.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseLysosomal dysfunction
    Study

    mousen: not reported in source

    LPS-induced sepsis
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    500 mg/kg · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    NMN administration attenuated LPS-induced deteriorative effects.
    3 context sentences
    Summary · context
    We showed that LPS treatment markedly increased mitochondrial ROS production and induced lysosomal dysfunction and aberrant autophagy in cardiomyocytes and mouse hearts, leading to inflammatory responses and myocardial injury and dysfunction in septic mice.
    Summary · context
    Sepsis was induced in mice by injection of LPS (4 mg/kg, i.p.).
    Summary · context
    Then mice received NMN (500 mg/kg, i.p.) or mito-TEMPO (0.7 mg/kg, i.p.) right after LPS injection, and subjected to echocardiography for assessing myocardial function.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In septic mouse hearts, NMN attenuated LPS-induced aberrant autophagy.

    In plain wordsIn mice with sepsis, NMN reduced abnormal autophagy in hearts.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseAberrant autophagy
    Study

    mousen: not reported in source

    LPS-induced sepsis
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    500 mg/kg · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    NMN administration attenuated LPS-induced deteriorative effects.
    3 context sentences
    Summary · context
    We showed that LPS treatment markedly increased mitochondrial ROS production and induced lysosomal dysfunction and aberrant autophagy in cardiomyocytes and mouse hearts, leading to inflammatory responses and myocardial injury and dysfunction in septic mice.
    Summary · context
    Sepsis was induced in mice by injection of LPS (4 mg/kg, i.p.).
    Summary · context
    Then mice received NMN (500 mg/kg, i.p.) or mito-TEMPO (0.7 mg/kg, i.p.) right after LPS injection, and subjected to echocardiography for assessing myocardial function.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In septic mice, NMN attenuated LPS-induced inflammatory responses.

    In plain wordsIn mice with sepsis, NMN reduced LPS-induced inflammation.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseInflammatory responses
    Study

    mousen: not reported in source

    LPS-induced sepsis
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    500 mg/kg · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    NMN administration attenuated LPS-induced deteriorative effects.
    3 context sentences
    Summary · context
    We showed that LPS treatment markedly increased mitochondrial ROS production and induced lysosomal dysfunction and aberrant autophagy in cardiomyocytes and mouse hearts, leading to inflammatory responses and myocardial injury and dysfunction in septic mice.
    Summary · context
    Sepsis was induced in mice by injection of LPS (4 mg/kg, i.p.).
    Summary · context
    Then mice received NMN (500 mg/kg, i.p.) or mito-TEMPO (0.7 mg/kg, i.p.) right after LPS injection, and subjected to echocardiography for assessing myocardial function.
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In septic mice, NMN attenuated LPS-induced myocardial injury.

    In plain wordsIn mice with sepsis, NMN reduced LPS-induced heart injury.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseMyocardial injury
    Study

    mousen: not reported in source

    LPS-induced sepsis
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    500 mg/kg · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    NMN administration attenuated LPS-induced deteriorative effects.
    3 context sentences
    Summary · context
    We showed that LPS treatment markedly increased mitochondrial ROS production and induced lysosomal dysfunction and aberrant autophagy in cardiomyocytes and mouse hearts, leading to inflammatory responses and myocardial injury and dysfunction in septic mice.
    Summary · context
    Sepsis was induced in mice by injection of LPS (4 mg/kg, i.p.).
    Summary · context
    Then mice received NMN (500 mg/kg, i.p.) or mito-TEMPO (0.7 mg/kg, i.p.) right after LPS injection, and subjected to echocardiography for assessing myocardial function.
  6. 06AnimalAnimal study (in vivo)Efficacy outcome

    In septic mice, NMN attenuated LPS-induced myocardial dysfunction.

    In plain wordsIn mice with sepsis, NMN reduced LPS-induced heart dysfunction.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseMyocardial dysfunction
    Study

    mousen: not reported in source

    LPS-induced sepsis
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    500 mg/kg · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    NMN administration attenuated LPS-induced deteriorative effects.
    3 context sentences
    Summary · context
    We showed that LPS treatment markedly increased mitochondrial ROS production and induced lysosomal dysfunction and aberrant autophagy in cardiomyocytes and mouse hearts, leading to inflammatory responses and myocardial injury and dysfunction in septic mice.
    Summary · context
    Sepsis was induced in mice by injection of LPS (4 mg/kg, i.p.).
    Summary · context
    Then mice received NMN (500 mg/kg, i.p.) or mito-TEMPO (0.7 mg/kg, i.p.) right after LPS injection, and subjected to echocardiography for assessing myocardial function.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In septic mouse hearts, NMN prevented the LPS-induced increase in PPIF acetylation.

    In plain wordsIn mice with sepsis, NMN prevented increased PPIF acetylation in hearts.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreasePPIF acetylation
    Study

    mousen: not reported in source

    LPS-induced sepsis
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    500 mg/kg · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    Notably, LPS treatment significantly increased acetylation and oxidation of PPIF, which was prevented by NMN in mouse hearts.
    2 context sentences
    Summary · context
    Sepsis was induced in mice by injection of LPS (4 mg/kg, i.p.).
    Summary · context
    Then mice received NMN (500 mg/kg, i.p.) or mito-TEMPO (0.7 mg/kg, i.p.) right after LPS injection, and subjected to echocardiography for assessing myocardial function.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In septic mouse hearts, NMN prevented the LPS-induced increase in PPIF oxidation.

    In plain wordsIn mice with sepsis, NMN prevented increased PPIF oxidation in hearts.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreasePPIF oxidation
    Study

    mousen: not reported in source

    LPS-induced sepsis
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    500 mg/kg · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    Notably, LPS treatment significantly increased acetylation and oxidation of PPIF, which was prevented by NMN in mouse hearts.
    2 context sentences
    Summary · context
    Sepsis was induced in mice by injection of LPS (4 mg/kg, i.p.).
    Summary · context
    Then mice received NMN (500 mg/kg, i.p.) or mito-TEMPO (0.7 mg/kg, i.p.) right after LPS injection, and subjected to echocardiography for assessing myocardial function.
  9. 09AnimalAnimal study (in vivo)Mechanism

    In septic mouse hearts, NMN abrogated LPS-induced ATP5A1 acetylation.

    In plain wordsIn mice with sepsis, NMN prevented LPS-induced ATP5A1 acetylation in hearts.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseATP5A1 acetylation
    Study

    mousen: not reported in source

    LPS-induced sepsis
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    500 mg/kg · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    In addition, administration of NMN abrogated LPS-induced ATP5A1 acetylation and increased ATP5A1 protein levels and ATP production in septic mouse hearts.
    2 context sentences
    Summary · context
    Sepsis was induced in mice by injection of LPS (4 mg/kg, i.p.).
    Summary · context
    Then mice received NMN (500 mg/kg, i.p.) or mito-TEMPO (0.7 mg/kg, i.p.) right after LPS injection, and subjected to echocardiography for assessing myocardial function.
  10. 10AnimalAnimal study (in vivo)Mechanism

    In septic mouse hearts, NMN increased ATP5A1 protein levels.

    In plain wordsIn mice with sepsis, NMN increased ATP5A1 protein in hearts.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseATP5A1 protein
    Study

    mousen: not reported in source

    LPS-induced sepsis
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    500 mg/kg · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    In addition, administration of NMN abrogated LPS-induced ATP5A1 acetylation and increased ATP5A1 protein levels and ATP production in septic mouse hearts.
    2 context sentences
    Summary · context
    Sepsis was induced in mice by injection of LPS (4 mg/kg, i.p.).
    Summary · context
    Then mice received NMN (500 mg/kg, i.p.) or mito-TEMPO (0.7 mg/kg, i.p.) right after LPS injection, and subjected to echocardiography for assessing myocardial function.
  11. 11AnimalAnimal study (in vivo)Mechanism

    In septic mouse hearts, NMN increased ATP production.

    In plain wordsIn mice with sepsis, NMN increased ATP production in hearts.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseATP production
    Study

    mousen: not reported in source

    LPS-induced sepsis
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    500 mg/kg · intraperitonealAs given in this study (mouse).

    Source sentences

    Summary
    In addition, administration of NMN abrogated LPS-induced ATP5A1 acetylation and increased ATP5A1 protein levels and ATP production in septic mouse hearts.
    2 context sentences
    Summary · context
    Sepsis was induced in mice by injection of LPS (4 mg/kg, i.p.).
    Summary · context
    Then mice received NMN (500 mg/kg, i.p.) or mito-TEMPO (0.7 mg/kg, i.p.) right after LPS injection, and subjected to echocardiography for assessing myocardial function.
  12. 12LabIn vitro (cells)Mechanism

    In neonatal mouse cardiomyocytes, NMN attenuated LPS-induced mitochondrial ROS production.

    In plain wordsIn cells from newborn mouse hearts, NMN reduced LPS-induced mitochondrial reactive oxygen production.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseMitochondrial ROS
    Study

    mousen: not reported in source

    LPS-treated neonatal mouse cardiomyocytes
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    500 µmol/LAs given in this study (mouse).

    Source sentences

    Summary
    NMN administration attenuated LPS-induced deteriorative effects.
    2 context sentences
    Summary · context
    We showed that LPS treatment markedly increased mitochondrial ROS production and induced lysosomal dysfunction and aberrant autophagy in cardiomyocytes and mouse hearts, leading to inflammatory responses and myocardial injury and dysfunction in septic mice.
    Summary · context
    In vitro experiments were conducted in neonatal mouse cardiomyocytes treated with LPS (1 µg/mL) in the presence of NMN (500 µmol/L) or mito-TEMPO (25 nmol/L).
  13. 13LabIn vitro (cells)Mechanism

    In neonatal mouse cardiomyocytes, NMN attenuated LPS-induced lysosomal dysfunction.

    In plain wordsIn cells from newborn mouse hearts, NMN reduced LPS-induced lysosomal dysfunction.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseLysosomal dysfunction
    Study

    mousen: not reported in source

    LPS-treated neonatal mouse cardiomyocytes
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    500 µmol/LAs given in this study (mouse).

    Source sentences

    Summary
    NMN administration attenuated LPS-induced deteriorative effects.
    2 context sentences
    Summary · context
    We showed that LPS treatment markedly increased mitochondrial ROS production and induced lysosomal dysfunction and aberrant autophagy in cardiomyocytes and mouse hearts, leading to inflammatory responses and myocardial injury and dysfunction in septic mice.
    Summary · context
    In vitro experiments were conducted in neonatal mouse cardiomyocytes treated with LPS (1 µg/mL) in the presence of NMN (500 µmol/L) or mito-TEMPO (25 nmol/L).
  14. 14LabIn vitro (cells)Mechanism

    In neonatal mouse cardiomyocytes, NMN attenuated LPS-induced aberrant autophagy.

    In plain wordsIn cells from newborn mouse hearts, NMN reduced LPS-induced abnormal autophagy.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseAberrant autophagy
    Study

    mousen: not reported in source

    LPS-treated neonatal mouse cardiomyocytes
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    500 µmol/LAs given in this study (mouse).

    Source sentences

    Summary
    NMN administration attenuated LPS-induced deteriorative effects.
    2 context sentences
    Summary · context
    We showed that LPS treatment markedly increased mitochondrial ROS production and induced lysosomal dysfunction and aberrant autophagy in cardiomyocytes and mouse hearts, leading to inflammatory responses and myocardial injury and dysfunction in septic mice.
    Summary · context
    In vitro experiments were conducted in neonatal mouse cardiomyocytes treated with LPS (1 µg/mL) in the presence of NMN (500 µmol/L) or mito-TEMPO (25 nmol/L).

Studies that did not test the peptide alone1

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

  1. 15AnimalNot a test of NMN (nicotinamide mononucleotide) aloneAnimal study (in vivo)Mechanism

    In sepsis experiments, PPIF knockdown replicated NMN-associated benefits on ROS production, lysosomal dysfunction, abnormal autophagy, and myocardial injury and dysfunction.

    In plain wordsIn mice, PPIF knockdown reproduced the reported NMN benefits on reactive oxygen production, lysosomes, autophagy, and heart injury and function.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    Direction not reportedPPIF knockdown effects
    Study

    mousen: not reported in source

    Sepsis
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Knockdown of PPIF replicated the beneficial effects of NMN or mito-TEMPO on ROS production, lysosomal dysfunction, aberrant autophagy, and myocardial injury/dysfunction in sepsis.

    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 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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