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Study · Animal study (in vivo) · mouse · 2016

11 results

Nicotinamide mononucleotide supplementation reverses vascular dysfunction and oxidative stress with aging in mice.

de Picciotto NE, Gano LB, Johnson LC, Martens CR, Sindler AL, Mills KF, Imai S, Seals DR

Aging cell11 Mar 2016Cited by 338 (Europe PMC)

Summary

We tested the hypothesis that supplementation of nicotinamide mononucleotide (NMN), a key NAD(+) intermediate, increases arterial SIRT1 activity and reverses age-associated arterial dysfunction and oxidative stress. Old control mice (OC) had impaired carotid artery endothelium-dependent dilation (EDD) (60 ± 5% vs. 84 ± 2%), a measure of endothelial function, and nitric oxide (NO)-mediated EDD (37 ± 4% vs. 66 ± 6%), compared with young mice (YC). This age-associated impairment in EDD was restored in OC by the superoxide (O2-) scavenger TEMPOL (82 ± 7%). OC also had increased aortic pulse wave velocity (aPWV, 464 ± 31 cm s(-1) vs. 337 ± 3 cm s(-1) ) and elastic modulus (EM, 6407 ± 876 kPa vs. 3119 ± 471 kPa), measures of large elastic artery stiffness, compared with YC. OC had greater aortic O2- production (2.0 ± 0.1 vs. 1.0 ± 0.1 AU), nitrotyrosine abundance (a marker of oxidative stress), and collagen-I, and reduced elastin and vascular SIRT1 activity, measured by the acetylation status of the p65 subunit of NFκB, compared with YC. Supplementation with NMN in old mice restored EDD (86 ± 2%) and NO-mediated EDD (61 ± 5%), reduced aPWV (359 ± 14 cm s(-1) ) and EM (3694 ± 315 kPa), normalized O2- production (0.9 ± 0.1 AU), decreased nitrotyrosine, reversed collagen-I, increased elastin, and restored vascular SIRT1 activity. Acute NMN incubation in isolated aortas increased NAD(+) threefold and manganese superoxide dismutase (MnSOD) by 50%. NMN supplementation may represent a novel therapy to restore SIRT1 activity and reverse age-related arterial dysfunction by decreasing oxidative stress.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study11

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In old mice, NMN restored endothelium-dependent dilation.

    In plain wordsIn old mice, NMN restored artery dilation compared with old controls.

    Outcome
    IncreaseEndothelium-dependent dilation
    Study

    mousen: not reported in source

    old mice
    Comparator
    old control mice
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Measurements

    EDD
    86%
    NMN-treated old mice

    Source sentences

    Summary
    Supplementation with NMN in old mice restored EDD (86 ± 2%) and NO-mediated EDD (61 ± 5%),
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In old mice, NMN restored nitric oxide-mediated endothelium-dependent dilation.

    In plain wordsIn old mice, NMN restored nitric oxide-mediated artery dilation compared with old controls.

    Outcome
    IncreaseNO-mediated endothelium-dependent dilation
    Study

    mousen: not reported in source

    old mice
    Comparator
    old control mice
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Measurements

    NO-mediated EDD
    61%
    NMN-treated old mice

    Source sentences

    Summary
    Supplementation with NMN in old mice restored EDD (86 ± 2%) and NO-mediated EDD (61 ± 5%),
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In old mice, NMN reduced aortic pulse wave velocity.

    In plain wordsIn old mice, NMN reduced a measure of artery stiffness compared with old controls.

    Outcome
    DecreaseAortic pulse wave velocity
    Study

    mousen: not reported in source

    old mice
    Comparator
    old control mice
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Measurements

    aPWV
    359 cm s(-1)
    NMN-treated old mice

    Source sentences

    Summary
    reduced aPWV (359 ± 14 cm s(-1) ) and EM (3694 ± 315 kPa),
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In old mice, NMN reduced arterial elastic modulus.

    In plain wordsIn old mice, NMN reduced arterial elastic modulus compared with old controls.

    Outcome
    DecreaseElastic modulus
    Study

    mousen: not reported in source

    old mice
    Comparator
    old control mice
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Measurements

    EM
    3694 kPa
    NMN-treated old mice

    Source sentences

    Summary
    reduced aPWV (359 ± 14 cm s(-1) ) and EM (3694 ± 315 kPa),
  5. 05AnimalAnimal study (in vivo)Mechanism

    In old mice, NMN normalized aortic superoxide production.

    In plain wordsIn old mice, NMN normalized artery superoxide production compared with old controls.

    Outcome
    DecreaseAortic superoxide production
    Study

    mousen: not reported in source

    old mice
    Comparator
    old control mice
    Outcome group
    Oxidative stress · Cardiovascular
    Studied dose
    Dose not stated

    Measurements

    O2- production
    0.9 AU
    NMN-treated old mice

    Source sentences

    Summary
    normalized O2- production (0.9 ± 0.1 AU), decreased nitrotyrosine, reversed collagen-I, increased elastin, and restored vascular SIRT1 activity.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In old mice, NMN decreased nitrotyrosine abundance.

    In plain wordsIn old mice, NMN reduced nitrotyrosine compared with old controls.

    Outcome
    DecreaseNitrotyrosine abundance
    Study

    mousen: not reported in source

    old mice
    Comparator
    old control mice
    Outcome group
    Oxidative stress · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    normalized O2- production (0.9 ± 0.1 AU), decreased nitrotyrosine, reversed collagen-I, increased elastin, and restored vascular SIRT1 activity.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In old mice, NMN reversed the age-associated increase in collagen-I.

    In plain wordsIn old mice, NMN reversed increased artery collagen-I compared with old controls.

    Outcome
    DecreaseCollagen-I abundance
    Study

    mousen: not reported in source

    old mice
    Comparator
    old control mice
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    normalized O2- production (0.9 ± 0.1 AU), decreased nitrotyrosine, reversed collagen-I, increased elastin, and restored vascular SIRT1 activity.
    1 context sentence
    Summary · context
    OC had greater aortic O2- production (2.0 ± 0.1 vs. 1.0 ± 0.1 AU), nitrotyrosine abundance (a marker of oxidative stress), and collagen-I, and reduced elastin and vascular SIRT1 activity, measured by the acetylation status of the p65 subunit of NFκB, compared with YC.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In old mice, NMN increased elastin.

    In plain wordsIn old mice, NMN increased artery elastin compared with old controls.

    Outcome
    IncreaseElastin abundance
    Study

    mousen: not reported in source

    old mice
    Comparator
    old control mice
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    normalized O2- production (0.9 ± 0.1 AU), decreased nitrotyrosine, reversed collagen-I, increased elastin, and restored vascular SIRT1 activity.
  9. 09AnimalAnimal study (in vivo)Mechanism

    In old mice, NMN restored vascular SIRT1 activity.

    In plain wordsIn old mice, NMN restored artery SIRT1 activity compared with old controls.

    Outcome
    IncreaseVascular SIRT1 activity
    Study

    mousen: not reported in source

    old mice
    Comparator
    old control mice
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    normalized O2- production (0.9 ± 0.1 AU), decreased nitrotyrosine, reversed collagen-I, increased elastin, and restored vascular SIRT1 activity.
  10. 10LabEx vivo tissueMechanism

    In isolated mouse aortas, acute NMN incubation increased NAD threefold.

    In plain wordsIn lab tests, acute NMN exposure increased NAD threefold in isolated mouse arteries.

    Outcome
    IncreaseAortic NAD levels
    Study

    mousen: not reported in source

    isolated mouse aortas
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Measurements

    NAD increase
    3 fold
    acute NMN incubation

    Source sentences

    Summary
    Acute NMN incubation in isolated aortas increased NAD(+) threefold and manganese superoxide dismutase (MnSOD) by 50%.
  11. 11LabEx vivo tissueMechanism

    In isolated mouse aortas, acute NMN incubation increased manganese superoxide dismutase by 50%.

    In plain wordsIn lab tests, acute NMN exposure increased manganese superoxide dismutase by 50% in isolated mouse arteries.

    Outcome
    IncreaseMnSOD
    Study

    mousen: not reported in source

    isolated mouse aortas
    Outcome group
    Oxidative stress · Cardiovascular
    Studied dose
    Dose not stated

    Measurements

    MnSOD increase
    50%
    acute NMN incubation

    Source sentences

    Summary
    Acute NMN incubation in isolated aortas increased NAD(+) threefold and manganese superoxide dismutase (MnSOD) by 50%.

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

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