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Study · Animal study (in vivo) · mouse · 2023

14 results

Nicotinamide Mononucleotide Alleviates Osteoblast Senescence Induction and Promotes Bone Healing in Osteoporotic Mice.

Lu Z, Jiang L, Lesani P, Zhang W, Li N, Luo D, Li Y, Ye Y, Bian J, Wang G, Dunstan CR, Jiang X, Zreiqat H

The journals of gerontology. Series A, Biological sciences and medical sciences1 Feb 2023Cited by 23 (Europe PMC)

PMID36037105 (opens in a new tab)DOI10.1093/gerona/glac175 (opens in a new tab)PepBankPUB-36037105
Publisher pagePubMedAsk about this study
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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 study14

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In mice, NMN attenuated senescent cell induction in growth plates.

    In plain wordsIn mice, NMN reduced senescent cell induction in bone growth plates.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseGrowth plate senescence
    Study

    mousen: not reported in source

    In vivo growth plates
    Outcome group
    Aging markers · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vivo, NMN supplementation attenuates senescent cell induction in growth plates, partially prevents osteoporosis in an ovariectomized mouse model, and accelerates bone healing in osteoporotic mice.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In ovariectomized mice, NMN partially prevented osteoporosis.

    In plain wordsIn mice with removed ovaries, NMN partly prevented osteoporosis.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseOsteoporosis
    Study

    mousen: not reported in source

    Ovariectomized mouse model
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vivo, NMN supplementation attenuates senescent cell induction in growth plates, partially prevents osteoporosis in an ovariectomized mouse model, and accelerates bone healing in osteoporotic mice.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In osteoporotic mice, NMN accelerated bone healing.

    In plain wordsIn mice with osteoporosis, NMN accelerated bone healing.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseBone healing
    Study

    mousen: not reported in source

    Osteoporotic mice
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vivo, NMN supplementation attenuates senescent cell induction in growth plates, partially prevents osteoporosis in an ovariectomized mouse model, and accelerates bone healing in osteoporotic mice.
  4. 04LabIn vitro (cells)Mechanism

    In human primary osteoblasts, NMN partially reversed TNF-α-induced senescence.

    In plain wordsIn cells, NMN partly reversed osteoblast senescence compared with TNF-α alone.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseOsteoblast senescence
    Study

    humann: not reported in source

    TNF-α-treated human primary osteoblasts
    Comparator
    TNF-α without NMN
    Outcome group
    Aging markers · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we show that NMN treatment partially reverses the effects of tumor necrosis factor-alpha (TNF-α) on human primary osteoblasts (HOBs): senescent cell induction, diminished osteogenic differentiation ability, and intracellular NAD+ and NADH levels.
  5. 05LabIn vitro (cells)Mechanism

    In human primary osteoblasts, NMN partially reversed TNF-α-induced loss of osteogenic differentiation ability.

    In plain wordsIn cells, NMN partly restored bone-forming differentiation compared with TNF-α alone.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseOsteogenic differentiation
    Study

    humann: not reported in source

    TNF-α-treated human primary osteoblasts
    Comparator
    TNF-α without NMN
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we show that NMN treatment partially reverses the effects of tumor necrosis factor-alpha (TNF-α) on human primary osteoblasts (HOBs): senescent cell induction, diminished osteogenic differentiation ability, and intracellular NAD+ and NADH levels.
  6. 06LabIn vitro (cells)Mechanism

    In human primary osteoblasts, NMN partially reversed TNF-α effects on intracellular NAD levels.

    In plain wordsIn cells, NMN partly reversed NAD level changes compared with TNF-α alone.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    Direction not reportedIntracellular NAD levels
    Study

    humann: not reported in source

    TNF-α-treated human primary osteoblasts
    Comparator
    TNF-α without NMN
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we show that NMN treatment partially reverses the effects of tumor necrosis factor-alpha (TNF-α) on human primary osteoblasts (HOBs): senescent cell induction, diminished osteogenic differentiation ability, and intracellular NAD+ and NADH levels.
  7. 07LabIn vitro (cells)Mechanism

    In human primary osteoblasts, NMN partially reversed TNF-α effects on intracellular NADH levels.

    In plain wordsIn cells, NMN partly reversed NADH level changes compared with TNF-α alone.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    Direction not reportedIntracellular NADH levels
    Study

    humann: not reported in source

    TNF-α-treated human primary osteoblasts
    Comparator
    TNF-α without NMN
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we show that NMN treatment partially reverses the effects of tumor necrosis factor-alpha (TNF-α) on human primary osteoblasts (HOBs): senescent cell induction, diminished osteogenic differentiation ability, and intracellular NAD+ and NADH levels.
  8. 08LabIn vitro (cells)Mechanism

    In human primary osteoblasts, NMN increased mitochondrial membrane potential after TNF-α exposure.

    In plain wordsIn cells, NMN increased mitochondrial membrane potential compared with TNF-α alone.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseMitochondrial membrane potential
    Study

    humann: not reported in source

    TNF-α-treated human primary osteoblasts
    Comparator
    TNF-α without NMN
    Outcome group
    Mitochondrial function · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, NMN restores the mitochondrial dysfunction in HOBs induced by TNF-α evidenced by increased mitochondrial membrane potential and reduced reactive oxidative species and mitochondrial mass.
  9. 09LabIn vitro (cells)Mechanism

    In human primary osteoblasts, NMN reduced reactive oxidative species after TNF-α exposure.

    In plain wordsIn cells, NMN reduced reactive oxidative species compared with TNF-α alone.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseReactive oxidative species
    Study

    humann: not reported in source

    TNF-α-treated human primary osteoblasts
    Comparator
    TNF-α without NMN
    Outcome group
    Mitochondrial function · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, NMN restores the mitochondrial dysfunction in HOBs induced by TNF-α evidenced by increased mitochondrial membrane potential and reduced reactive oxidative species and mitochondrial mass.
  10. 10LabIn vitro (cells)Mechanism

    In human primary osteoblasts, NMN reduced mitochondrial mass after TNF-α exposure.

    In plain wordsIn cells, NMN reduced mitochondrial mass compared with TNF-α alone.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseMitochondrial mass
    Study

    humann: not reported in source

    TNF-α-treated human primary osteoblasts
    Comparator
    TNF-α without NMN
    Outcome group
    Mitochondrial function · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, NMN restores the mitochondrial dysfunction in HOBs induced by TNF-α evidenced by increased mitochondrial membrane potential and reduced reactive oxidative species and mitochondrial mass.
  11. 11LabIn vitro (cells)Mechanism

    In human primary osteoblasts, NMN increased mitophagy activity.

    In plain wordsIn cells, NMN increased mitochondrial recycling compared with TNF-α alone.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseMitophagy activity
    Study

    humann: not reported in source

    TNF-α-treated human primary osteoblasts
    Comparator
    TNF-α without NMN
    Outcome group
    Mitochondrial function · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN also increases mitophagy activity by down-regulating P62 expression and up-regulating light chain 3B-II protein expression.
  12. 12LabIn vitro (cells)Mechanism

    In human primary osteoblasts, NMN reduced P62 expression.

    In plain wordsIn cells, NMN reduced P62 expression compared with TNF-α alone.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseP62 expression
    Study

    humann: not reported in source

    TNF-α-treated human primary osteoblasts
    Comparator
    TNF-α without NMN
    Outcome group
    Mitochondrial function · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN also increases mitophagy activity by down-regulating P62 expression and up-regulating light chain 3B-II protein expression.
  13. 13LabIn vitro (cells)Mechanism

    In human primary osteoblasts, NMN increased light chain 3B-II protein expression.

    In plain wordsIn cells, NMN increased light chain 3B-II protein expression compared with TNF-α alone.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    IncreaseLight chain 3B-II expression
    Study

    humann: not reported in source

    TNF-α-treated human primary osteoblasts
    Comparator
    TNF-α without NMN
    Outcome group
    Mitochondrial function · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    NMN also increases mitophagy activity by down-regulating P62 expression and up-regulating light chain 3B-II protein expression.

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. 14LabNot a test of NMN (nicotinamide mononucleotide) aloneIn vitro (cells)Mechanism

    In human primary osteoblasts, Bafilomycin A1 mitigated NMN protection against senescence.

    In plain wordsIn cells, a mitophagy inhibitor reduced NMN protection against senescence compared with NMN without the inhibitor.

    Peptide
    NMN (nicotinamide mononucleotide)
    Outcome
    DecreaseMitophagy inhibition of senescence protection
    Study

    humann: not reported in source

    TNF-α-treated human primary osteoblasts
    Comparator
    NMN without Bafilomycin A1
    Outcome group
    Aging markers · Musculoskeletal

    Source sentences

    Summary
    In addition, the cell senescence protective effects of NMN on HOBs are mitigated by a mitophagy inhibitor (Bafilomycin A1).

    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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