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Study · Animal study (in vivo) · mouse · 2024

10 results

The Mitochondrial-Derived Peptide MOTS-c Alleviates Radiation Pneumonitis via an Nrf2-Dependent Mechanism.

Zhang Y, Huang J, Zhang Y, Jiang F, Li S, He S, Sun J, Chen D, Tong Y, Pang Q, Wu Y

Antioxidants (Basel, Switzerland)17 May 2024Cited by 22 (Europe PMC)

PMID38790718 (opens in a new tab)PMCIDPMC11117534 (opens in a new tab)DOI10.3390/antiox13050613 (opens in a new tab)PepBankPUB-38790718
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Summary

Radiation pneumonitis (RP) is a prevalent and fatal complication of thoracic radiotherapy due to the lack of effective treatment options. RP primarily arises from mitochondrial injury in lung epithelial cells. The mitochondrial-derived peptide MOTS-c has demonstrated protective effects against various diseases by mitigating mitochondrial injury. C57BL/6 mice were exposed to 20 Gy of lung irradiation (IR) and received daily intraperitoneal injections of MOTS-c for 2 weeks. MOTS-c significantly ameliorated lung tissue damage, inflammation, and oxidative stress caused by radiation. Meanwhile, MOTS-c reversed the apoptosis and mitochondrial damage of alveolar epithelial cells in RP mice. Furthermore, MOTS-c significantly inhibited oxidative stress and mitochondrial damage in MLE-12 cells and primary mouse lung epithelial cells. Mechanistically, MOTS-c increased the nuclear factor erythroid 2-related factor (Nrf2) level and promoted its nuclear translocation. Notably, Nrf2 deficiency abolished the protective function of MOTS-c in mice with RP. In conclusion, MOTS-c alleviates RP by protecting mitochondrial function through an Nrf2-dependent mechanism, indicating that MOTS-c may be a novel potential protective agent against RP.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study10

10 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 radiation pneumonitis, MOTS‑c ameliorated lung tissue damage caused by radiation.

    In plain wordsIn mice with radiation lung injury, MOTS‑c reduced lung tissue damage.

    Peptide
    MOTS-c
    Outcome
    DecreaseRadiation-induced lung tissue damage
    Study

    mousen: not reported in source

    Radiation pneumonitis (20 Gy lung irradiation)
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated · intraperitoneal · 2 weeksAs given in this study (mouse).

    Source sentences

    Summary
    MOTS-c significantly ameliorated lung tissue damage, inflammation, and oxidative stress caused by radiation.
    1 context sentence
    Summary · context
    C57BL/6 mice were exposed to 20 Gy of lung irradiation (IR) and received daily intraperitoneal injections of MOTS-c for 2 weeks.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice with radiation pneumonitis, MOTS‑c ameliorated inflammation caused by radiation.

    In plain wordsIn mice with radiation lung injury, MOTS‑c reduced lung inflammation.

    Peptide
    MOTS-c
    Outcome
    DecreaseRadiation-induced lung inflammation
    Study

    mousen: not reported in source

    Radiation pneumonitis (20 Gy lung irradiation)
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated · intraperitoneal · 2 weeksAs given in this study (mouse).

    Source sentences

    Summary
    MOTS-c significantly ameliorated lung tissue damage, inflammation, and oxidative stress caused by radiation.
    1 context sentence
    Summary · context
    C57BL/6 mice were exposed to 20 Gy of lung irradiation (IR) and received daily intraperitoneal injections of MOTS-c for 2 weeks.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mice with radiation pneumonitis, MOTS‑c ameliorated oxidative stress caused by radiation.

    In plain wordsIn mice with radiation lung injury, MOTS‑c reduced oxidative stress.

    Peptide
    MOTS-c
    Outcome
    DecreaseRadiation-induced oxidative stress in lung
    Study

    mousen: not reported in source

    Radiation pneumonitis (20 Gy lung irradiation)
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated · intraperitoneal · 2 weeksAs given in this study (mouse).

    Source sentences

    Summary
    MOTS-c significantly ameliorated lung tissue damage, inflammation, and oxidative stress caused by radiation.
    1 context sentence
    Summary · context
    C57BL/6 mice were exposed to 20 Gy of lung irradiation (IR) and received daily intraperitoneal injections of MOTS-c for 2 weeks.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In mice with radiation pneumonitis, MOTS‑c reversed apoptosis of alveolar epithelial cells.

    In plain wordsIn mice with radiation lung injury, MOTS‑c reduced death of lung air-sac lining cells.

    Peptide
    MOTS-c
    Outcome
    DecreaseApoptosis of alveolar epithelial cells
    Study

    mousen: not reported in source

    Radiation pneumonitis (20 Gy lung irradiation)
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated · intraperitoneal · 2 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Meanwhile, MOTS-c reversed the apoptosis and mitochondrial damage of alveolar epithelial cells in RP mice.
    1 context sentence
    Summary · context
    C57BL/6 mice were exposed to 20 Gy of lung irradiation (IR) and received daily intraperitoneal injections of MOTS-c for 2 weeks.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In mice with radiation pneumonitis, MOTS‑c reversed mitochondrial damage of alveolar epithelial cells.

    In plain wordsIn mice with radiation lung injury, MOTS‑c reduced mitochondrial damage in lung air-sac lining cells.

    Peptide
    MOTS-c
    Outcome
    DecreaseMitochondrial damage of alveolar epithelial cells
    Study

    mousen: not reported in source

    Radiation pneumonitis (20 Gy lung irradiation)
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated · intraperitoneal · 2 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Meanwhile, MOTS-c reversed the apoptosis and mitochondrial damage of alveolar epithelial cells in RP mice.
    1 context sentence
    Summary · context
    C57BL/6 mice were exposed to 20 Gy of lung irradiation (IR) and received daily intraperitoneal injections of MOTS-c for 2 weeks.
  6. 06AnimalAnimal study (in vivo)Mechanism

    MOTS‑c increased the level of nuclear factor erythroid 2-related factor (Nrf2) in the radiation pneumonitis model.

    In plain wordsIn the lung-injury model, MOTS‑c raised levels of the protective protein Nrf2.

    Peptide
    MOTS-c
    Outcome
    IncreaseNrf2 level
    Study

    mousen: not reported in source

    Radiation pneumonitis (20 Gy lung irradiation)
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated · intraperitoneal · 2 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Mechanistically, MOTS-c increased the nuclear factor erythroid 2-related factor (Nrf2) level and promoted its nuclear translocation.
    1 context sentence
    Summary · context
    C57BL/6 mice were exposed to 20 Gy of lung irradiation (IR) and received daily intraperitoneal injections of MOTS-c for 2 weeks.
  7. 07AnimalAnimal study (in vivo)Mechanism

    MOTS‑c promoted nuclear translocation of Nrf2 in the radiation pneumonitis model.

    In plain wordsIn the lung-injury model, MOTS‑c helped Nrf2 move into the cell nucleus.

    Peptide
    MOTS-c
    Outcome
    IncreaseNrf2 nuclear translocation
    Study

    mousen: not reported in source

    Radiation pneumonitis (20 Gy lung irradiation)
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated · intraperitoneal · 2 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Mechanistically, MOTS-c increased the nuclear factor erythroid 2-related factor (Nrf2) level and promoted its nuclear translocation.
    1 context sentence
    Summary · context
    C57BL/6 mice were exposed to 20 Gy of lung irradiation (IR) and received daily intraperitoneal injections of MOTS-c for 2 weeks.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In mice with radiation pneumonitis, Nrf2 deficiency abolished the protective function of MOTS‑c.

    In plain wordsIn mice with radiation lung injury, MOTS‑c gave no protection when the Nrf2 protein was missing.

    Peptide
    MOTS-c
    Outcome
    No significant changeProtective effect of MOTS-c in Nrf2-deficient mice
    Study

    mousen: not reported in source

    Radiation pneumonitis (20 Gy lung irradiation)
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated · intraperitoneal · 2 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Notably, Nrf2 deficiency abolished the protective function of MOTS-c in mice with RP.
    1 context sentence
    Summary · context
    C57BL/6 mice were exposed to 20 Gy of lung irradiation (IR) and received daily intraperitoneal injections of MOTS-c for 2 weeks.
  9. 09LabIn vitro (cells)Mechanism

    In MLE-12 cells and primary mouse lung epithelial cells, MOTS‑c inhibited oxidative stress.

    In plain wordsIn lab-grown mouse lung cells, MOTS‑c reduced oxidative stress.

    Peptide
    MOTS-c
    Outcome
    DecreaseOxidative stress in MLE-12 and primary lung epithelial cells
    Study

    mousen: not reported in source

    MLE-12 cells and primary mouse lung epithelial cells
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, MOTS-c significantly inhibited oxidative stress and mitochondrial damage in MLE-12 cells and primary mouse lung epithelial cells.
  10. 10LabIn vitro (cells)Mechanism

    In MLE-12 cells and primary mouse lung epithelial cells, MOTS‑c inhibited mitochondrial damage.

    In plain wordsIn lab-grown mouse lung cells, MOTS‑c reduced mitochondrial damage.

    Peptide
    MOTS-c
    Outcome
    DecreaseMitochondrial damage in MLE-12 and primary lung epithelial cells
    Study

    mousen: not reported in source

    MLE-12 cells and primary mouse lung epithelial cells
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, MOTS-c significantly inhibited oxidative stress and mitochondrial damage in MLE-12 cells and primary mouse lung epithelial 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

    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.

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