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Study · Measured the body's own peptide · 2021

8 results

NAD+ supplementation prevents STING-induced senescence in ataxia telangiectasia by improving mitophagy.

Yang B, Dan X, Hou Y, Lee JH, Wechter N, Krishnamurthy S, Kimura R, Babbar M, Demarest T, McDevitt R, Zhang S, Zhang Y, Mattson MP, Croteau DL, Bohr VA

Aging cell18 Mar 2021Cited by 93 (Europe PMC)

PMID33734555 (opens in a new tab)PMCIDPMC8045911 (opens in a new tab)DOI10.1111/acel.13329 (opens in a new tab)PepBankPUB-33734555
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Summary

Senescence phenotypes and mitochondrial dysfunction are implicated in aging and in premature aging diseases, including ataxia telangiectasia (A-T). Loss of mitochondrial function can drive age-related decline in the brain, but little is known about whether improving mitochondrial homeostasis alleviates senescence phenotypes. We demonstrate here that mitochondrial dysfunction and cellular senescence with a senescence-associated secretory phenotype (SASP) occur in A-T patient fibroblasts, and in ATM-deficient cells and mice. Senescence is mediated by stimulator of interferon genes (STING) and involves ectopic cytoplasmic DNA. We further show that boosting intracellular NAD+ levels with nicotinamide riboside (NR) prevents senescence and SASP by promoting mitophagy in a PINK1-dependent manner. NR treatment also prevents neurodegeneration, suppresses senescence and neuroinflammation, and improves motor function in Atm-/- mice. Our findings suggest a central role for mitochondrial dysfunction-induced senescence in A-T pathogenesis, and that enhancing mitophagy as a potential therapeutic intervention.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study8

No result from this study comes from a test of the peptide.

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 01LabEndogenous levelIn vitro (cells)Mechanism

    In A-T experiments, NR boosted intracellular natural NAD+ levels.

    In plain wordsIn cells, NR increased natural intracellular NAD+ levels.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseIntracellular NAD+ levels
    Study

    n: not reported in source

    A-T experimental cells
    Outcome group
    Mitochondrial function · Aging and longevity

    Source sentences

    Summary
    We further show that boosting intracellular NAD+ levels with nicotinamide riboside (NR) prevents senescence and SASP by promoting mitophagy in a PINK1-dependent manner.

    This result measures the body's own NAD+ (nicotinamide adenine dinucleotide). Nobody was given the peptide. It is not evidence about taking it.

Studies that did not test the peptide alone7

In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).

  1. 02AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome

    In Atm-deficient mice, NR treatment prevented neurodegeneration.

    In plain wordsIn Atm-deficient mice, the NAD+ precursor NR prevented neurodegeneration.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseNeurodegeneration
    Study

    mousen: not reported in source

    Atm-/- mice
    Outcome group
    Neuroprotection · Nervous system and cognition

    Source sentences

    Summary
    NR treatment also prevents neurodegeneration, suppresses senescence and neuroinflammation, and improves motor function in Atm-/- mice.

    In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).

  2. 03AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome

    In Atm-deficient mice, NR treatment suppressed senescence.

    In plain wordsIn Atm-deficient mice, the NAD+ precursor NR suppressed senescence.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseSenescence suppression with NR
    Study

    mousen: not reported in source

    Atm-/- mice
    Outcome group
    Aging markers · Aging and longevity

    Source sentences

    Summary
    NR treatment also prevents neurodegeneration, suppresses senescence and neuroinflammation, and improves motor function in Atm-/- mice.

    In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).

  3. 04AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Mechanism

    In Atm-deficient mice, NR treatment suppressed neuroinflammation.

    In plain wordsIn Atm-deficient mice, the NAD+ precursor NR suppressed neuroinflammation.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseNeuroinflammation
    Study

    mousen: not reported in source

    Atm-/- mice
    Outcome group
    Inflammation markers · Nervous system and cognition

    Source sentences

    Summary
    NR treatment also prevents neurodegeneration, suppresses senescence and neuroinflammation, and improves motor function in Atm-/- mice.

    In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).

  4. 05AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneAnimal study (in vivo)Efficacy outcome

    In Atm-deficient mice, NR treatment improved motor function.

    In plain wordsIn Atm-deficient mice, the NAD+ precursor NR improved motor function.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreaseMotor function
    Study

    mousen: not reported in source

    Atm-/- mice
    Outcome group
    Exercise and physical function · Nervous system and cognition

    Source sentences

    Summary
    NR treatment also prevents neurodegeneration, suppresses senescence and neuroinflammation, and improves motor function in Atm-/- mice.

    In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).

  5. 06LabNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneIn vitro (cells)Efficacy outcome

    In A-T experiments, boosting intracellular NAD+ with NR prevented senescence.

    In plain wordsIn cells, the NAD+ precursor NR prevented senescence.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseSenescence prevention with NR
    Study

    n: not reported in source

    A-T experimental cells
    Outcome group
    Aging markers · Aging and longevity

    Source sentences

    Summary
    We further show that boosting intracellular NAD+ levels with nicotinamide riboside (NR) prevents senescence and SASP by promoting mitophagy in a PINK1-dependent manner.

    In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).

  6. 07LabNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneIn vitro (cells)Mechanism

    In A-T experiments, boosting intracellular NAD+ with NR prevented SASP.

    In plain wordsIn cells, the NAD+ precursor NR prevented SASP.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    DecreaseSASP prevention with NR
    Study

    n: not reported in source

    A-T experimental cells
    Outcome group
    Aging markers · Aging and longevity

    Source sentences

    Summary
    We further show that boosting intracellular NAD+ levels with nicotinamide riboside (NR) prevents senescence and SASP by promoting mitophagy in a PINK1-dependent manner.

    In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).

  7. 08LabNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneIn vitro (cells)Mechanism

    In A-T experiments, boosting NAD+ with NR promoted mitophagy in a PINK1-dependent manner.

    In plain wordsIn cells, the NAD+ precursor NR promoted mitophagy through a PINK1-dependent mechanism.

    Peptide
    NAD+ (nicotinamide adenine dinucleotide)
    Outcome
    IncreasePINK1-dependent mitophagy
    Study

    n: not reported in source

    A-T experimental cells
    Outcome group
    Mitochondrial function · Aging and longevity

    Source sentences

    Summary
    We further show that boosting intracellular NAD+ levels with nicotinamide riboside (NR) prevents senescence and SASP by promoting mitophagy in a PINK1-dependent manner.

    In this study, NAD+ (nicotinamide adenine dinucleotide) 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 NAD+ (nicotinamide adenine dinucleotide).

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

    14 Oct 2026, 05:02 UTC

    Study results updated

  2. Version 1

    14 Oct 2026, 01:46 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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