Skip to content

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

7 results

Nicotinamide Mononucleotide Attenuates Renal Interstitial Fibrosis After AKI by Suppressing Tubular DNA Damage and Senescence.

Jia Y, Kang X, Tan L, Ren Y, Qu L, Tang J, Liu G, Wang S, Xiong Z, Yang L

Frontiers in physiology23 Mar 2021Cited by 59 (Europe PMC)

PMID33833691 (opens in a new tab)PMCIDPMC8021789 (opens in a new tab)DOI10.3389/fphys.2021.649547 (opens in a new tab)PepBankPUB-33833691
Download PDFPubMedAsk about this study
Jump to 7 results

Summary

Acute kidney injury (AKI) is a worldwide health problem currently lacking therapeutics that directly promote renal repair or prevent the occurrence of chronic fibrosis. DNA damage is a feature of many forms of kidney injury, and targeting DNA damage and repair might be effective strategies for kidney protection in AKI. Boosting nicotinamide adenine dinucleotide (NAD+) levels is thought to have beneficial effects on DNA damage repair and fibrosis in other organs. However, no kidney-related studies of such effects have been performed to date. Here, we have shown that NMN (an NAD+ precursor) administration could significantly reduce tubular cell DNA damage and subsequent cellular senescence induced by hydrogen peroxide and hypoxia in human proximal tubular cells (HK-2 cells). The DNA damage inhibition, antiaging and anti-inflammatory effects of NMN were further confirmed in a unilateral ischemia-reperfusion injury (uIRI) mouse model. Most importantly, the antifibrosis activity of NMN was also shown in ischemic AKI mouse models, regardless of whether NMN was administered in advance or during the recovery phase. Collectively, these results suggest that NMN could significantly inhibit tubular cell DNA damage, senescence and inflammation. NMN administration might be an effective strategy for preventing or treating kidney fibrosis after AKI.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study7

7 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 unilateral ischemia-reperfusion injury, NMN inhibited DNA damage.

    In plain wordsIn mice with kidney ischemia-reperfusion injury, NMN reduced DNA damage.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseDNA damage
    Study

    mousen: not reported in source

    Unilateral ischemia-reperfusion injury
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The DNA damage inhibition, antiaging and anti-inflammatory effects of NMN were further confirmed in a unilateral ischemia-reperfusion injury (uIRI) mouse model.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice with unilateral ischemia-reperfusion injury, NMN showed antiaging effects.

    In plain wordsIn mice with kidney ischemia-reperfusion injury, NMN showed effects against cell aging.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseSenescence
    Study

    mousen: not reported in source

    Unilateral ischemia-reperfusion injury
    Outcome group
    Aging markers · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The DNA damage inhibition, antiaging and anti-inflammatory effects of NMN were further confirmed in a unilateral ischemia-reperfusion injury (uIRI) mouse model.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mice with unilateral ischemia-reperfusion injury, NMN showed anti-inflammatory effects.

    In plain wordsIn mice with kidney ischemia-reperfusion injury, NMN reduced inflammation.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseInflammation
    Study

    mousen: not reported in source

    Unilateral ischemia-reperfusion injury
    Outcome group
    Inflammation markers · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The DNA damage inhibition, antiaging and anti-inflammatory effects of NMN were further confirmed in a unilateral ischemia-reperfusion injury (uIRI) mouse model.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In mice with ischemic AKI, NMN showed antifibrosis activity when administered in advance.

    In plain wordsIn mice, NMN reduced kidney fibrosis when given before ischemic kidney injury.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseRenal fibrosis with preventive administration
    Study

    mousen: not reported in source

    Ischemic acute kidney injury
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Most importantly, the antifibrosis activity of NMN was also shown in ischemic AKI mouse models, regardless of whether NMN was administered in advance or during the recovery phase.
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In mice with ischemic AKI, NMN showed antifibrosis activity when administered during recovery.

    In plain wordsIn mice, NMN reduced kidney fibrosis when given during recovery from ischemic kidney injury.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseRenal fibrosis with recovery-phase administration
    Study

    mousen: not reported in source

    Ischemic acute kidney injury
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Most importantly, the antifibrosis activity of NMN was also shown in ischemic AKI mouse models, regardless of whether NMN was administered in advance or during the recovery phase.
  6. 06LabIn vitro (cells)Efficacy outcome

    In HK-2 cells, NMN significantly reduced tubular DNA damage induced by hydrogen peroxide and hypoxia.

    In plain wordsIn cells, NMN reduced kidney tubular DNA damage caused by hydrogen peroxide and hypoxia.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseTubular DNA damage
    Study

    humann: not reported in source

    HK-2 cells exposed to hydrogen peroxide and hypoxia
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here, we have shown that NMN (an NAD+ precursor) administration could significantly reduce tubular cell DNA damage and subsequent cellular senescence induced by hydrogen peroxide and hypoxia in human proximal tubular cells (HK-2 cells).
  7. 07LabIn vitro (cells)Efficacy outcome

    In HK-2 cells, NMN significantly reduced subsequent cellular senescence induced by hydrogen peroxide and hypoxia.

    In plain wordsIn cells, NMN reduced cell senescence caused by hydrogen peroxide and hypoxia.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseCellular senescence
    Study

    humann: not reported in source

    HK-2 cells exposed to hydrogen peroxide and hypoxia
    Outcome group
    Aging markers · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here, we have shown that NMN (an NAD+ precursor) administration could significantly reduce tubular cell DNA damage and subsequent cellular senescence induced by hydrogen peroxide and hypoxia in human proximal tubular cells (HK-2 cells).

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.

PepBank is a research reference. Talk to a doctor before you use any peptide.