Skip to content

Study · Animal study (in vivo) · mouse · 2026

13 results

Mitochondria-derived peptide MOTS-c alleviates hyperoxia-induced bronchopulmonary dysplasia in neonatal mice by activating Nrf2 pathway.

Chen D, Zhou MH, Zhu WY, Xing ZX, Li SP, Wu YX, Sun XL, Sun P, Pang QF

European journal of pharmacology7 Mar 2026

PMID41802484 (opens in a new tab)DOI10.1016/j.ejphar.2026.178726 (opens in a new tab)PepBankPUB-41802484
Publisher pagePubMedAsk about this study
Jump to 13 results

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 study13

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In neonatal mice with hyperoxia-induced BPD, exogenous MOTS‑c alleviated growth retardation.

    In plain wordsIn mice with a lung disease model, added MOTS‑c reduced stunted growth.

    Peptide
    MOTS-c
    Outcome
    DecreaseGrowth retardation
    Study

    mousen: not reported in source

    Hyperoxia-induced BPD
    Outcome group
    Body weight · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Exogenous MOTS-c supplementation alleviated growth retardation, attenuated alveolar simplification, and pulmonary vascular abnormalities in hyperoxia-induced BPD mice.
    1 context sentence
    Summary · context
    Here, hyperoxia (70% O2) was used to mimic the murine BPD model.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In neonatal mice with hyperoxia-induced BPD, exogenous MOTS‑c attenuated alveolar simplification.

    In plain wordsIn mice with a lung disease model, added MOTS‑c reduced the loss of fine lung structure.

    Peptide
    MOTS-c
    Outcome
    DecreaseAlveolar simplification
    Study

    mousen: not reported in source

    Hyperoxia-induced BPD
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Exogenous MOTS-c supplementation alleviated growth retardation, attenuated alveolar simplification, and pulmonary vascular abnormalities in hyperoxia-induced BPD mice.
    1 context sentence
    Summary · context
    Here, hyperoxia (70% O2) was used to mimic the murine BPD model.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In neonatal mice with hyperoxia-induced BPD, exogenous MOTS‑c attenuated pulmonary vascular abnormalities.

    In plain wordsIn mice with a lung disease model, added MOTS‑c reduced abnormal lung blood vessels.

    Peptide
    MOTS-c
    Outcome
    DecreasePulmonary vascular abnormalities
    Study

    mousen: not reported in source

    Hyperoxia-induced BPD
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Exogenous MOTS-c supplementation alleviated growth retardation, attenuated alveolar simplification, and pulmonary vascular abnormalities in hyperoxia-induced BPD mice.
    1 context sentence
    Summary · context
    Here, hyperoxia (70% O2) was used to mimic the murine BPD model.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In neonatal mice with hyperoxia-induced BPD, MOTS‑c administration significantly inhibited inflammation.

    In plain wordsIn mice with a lung disease model, MOTS‑c lowered inflammation.

    Peptide
    MOTS-c
    Outcome
    DecreaseInflammation in vivo
    Study

    mousen: not reported in source

    Hyperoxia-induced BPD
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MOTS-c administration significantly inhibited inflammation and oxidative stress both in vivo and in vitro.
    1 context sentence
    Summary · context
    Here, hyperoxia (70% O2) was used to mimic the murine BPD model.
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In neonatal mice with hyperoxia-induced BPD, MOTS‑c administration significantly inhibited oxidative stress.

    In plain wordsIn mice with a lung disease model, MOTS‑c lowered oxidative stress.

    Peptide
    MOTS-c
    Outcome
    DecreaseOxidative stress in vivo
    Study

    mousen: not reported in source

    Hyperoxia-induced BPD
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MOTS-c administration significantly inhibited inflammation and oxidative stress both in vivo and in vitro.
    1 context sentence
    Summary · context
    Here, hyperoxia (70% O2) was used to mimic the murine BPD model.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In Nrf2-deficient mice, the anti-inflammatory, anti-oxidative and pro-angiogenic effects of MOTS‑c were offset.

    In plain wordsIn mice without Nrf2, the protective effects of MOTS‑c were cancelled.

    Peptide
    MOTS-c
    Outcome
    Not applicableNrf2 dependence of MOTS-c effects in mice
    Study

    mousen: not reported in source

    Nrf2 deficiency mice
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    the beneficial effect of MOTS-c was Nrf2 dependent, since the anti-inflammation, anti-oxidative and pro-angiogenic effects of MOTS-c were offset in ML385 (a specific Nrf2 inhibitor) treated HUVECs or in Nrf2 deficiency mice.
  7. 07LabIn vitro (cells)Efficacy outcome

    In hyperoxia-stimulated HUVECs, MOTS‑c supplement increased cell viability.

    In plain wordsIn human blood vessel cells in the lab, MOTS‑c improved cell survival under high oxygen.

    Peptide
    MOTS-c
    Outcome
    IncreaseCell viability in hyperoxia-stimulated HUVECs
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Besides, MOTS-c supplement increased cell viability, inhibited cell death and promoted tube formation in hyperoxia-stimulated HUVECs.
  8. 08LabIn vitro (cells)Efficacy outcome

    In hyperoxia-stimulated HUVECs, MOTS‑c supplement inhibited cell death.

    In plain wordsIn human blood vessel cells in the lab, MOTS‑c reduced cell death under high oxygen.

    Peptide
    MOTS-c
    Outcome
    DecreaseCell death in hyperoxia-stimulated HUVECs
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Besides, MOTS-c supplement increased cell viability, inhibited cell death and promoted tube formation in hyperoxia-stimulated HUVECs.
  9. 09LabIn vitro (cells)Efficacy outcome

    In hyperoxia-stimulated HUVECs, MOTS‑c supplement promoted tube formation.

    In plain wordsIn human blood vessel cells in the lab, MOTS‑c helped the cells form vessel-like tubes under high oxygen.

    Peptide
    MOTS-c
    Outcome
    IncreaseTube formation in hyperoxia-stimulated HUVECs
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Besides, MOTS-c supplement increased cell viability, inhibited cell death and promoted tube formation in hyperoxia-stimulated HUVECs.
  10. 10LabIn vitro (cells)Efficacy outcome

    In hyperoxia-stimulated HUVECs, MOTS‑c administration significantly inhibited inflammation.

    In plain wordsIn human blood vessel cells in the lab, MOTS‑c lowered inflammation under high oxygen.

    Peptide
    MOTS-c
    Outcome
    DecreaseInflammation in vitro
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MOTS-c administration significantly inhibited inflammation and oxidative stress both in vivo and in vitro.
  11. 11LabIn vitro (cells)Efficacy outcome

    In hyperoxia-stimulated HUVECs, MOTS‑c administration significantly inhibited oxidative stress.

    In plain wordsIn human blood vessel cells in the lab, MOTS‑c lowered oxidative stress under high oxygen.

    Peptide
    MOTS-c
    Outcome
    DecreaseOxidative stress in vitro
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Oxidative stress · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MOTS-c administration significantly inhibited inflammation and oxidative stress both in vivo and in vitro.
  12. 12LabIn vitro (cells)Mechanism

    In HUVECs treated with the Nrf2 inhibitor ML385, the anti-inflammatory, anti-oxidative and pro-angiogenic effects of MOTS‑c were offset.

    In plain wordsIn human blood vessel cells in the lab, blocking Nrf2 cancelled the protective effects of MOTS‑c.

    Peptide
    MOTS-c
    Outcome
    Not applicableNrf2 dependence of MOTS-c effects in HUVECs
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    the beneficial effect of MOTS-c was Nrf2 dependent, since the anti-inflammation, anti-oxidative and pro-angiogenic effects of MOTS-c were offset in ML385 (a specific Nrf2 inhibitor) treated HUVECs or in Nrf2 deficiency mice.

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. 13AnimalEndogenous levelAnimal study (in vivo)Other

    MOTS‑c content was reduced in neonatal mice with hyperoxia-induced bronchopulmonary dysplasia.

    In plain wordsIn mice with a lung disease model, the body's own MOTS‑c level was lower.

    Peptide
    MOTS-c
    Outcome
    DecreaseMOTS-c content in hyperoxia-induced BPD
    Study

    mousen: not reported in source

    Hyperoxia-induced BPD
    Outcome group
    Mitochondrial function · Respiratory

    Source sentences

    Summary
    We found that MOTS-c content was reduced in hyperoxia-induced BPD mice.
    1 context sentence
    Summary · context
    Here, hyperoxia (70% O2) was used to mimic the murine BPD model.

    This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.

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

    10 Oct 2026, 08:19 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

Publication types

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