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

9 results

MOTS-c attenuates hyperoxia-induced neonatal cardiac injury by inhibiting oxeiptosis via maintaining the KEAP1-PGAM5 interaction.

Li SH, Chen SQ, Lu T, Wang JH, Wang JX, Wu YX, Pang QF, Chen D

Life sciences12 May 2026

PMID42128272 (opens in a new tab)DOI10.1016/j.lfs.2026.124452 (opens in a new tab)PepBankPUB-42128272
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 study9

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In hyperoxia-exposed neonatal mice, MOTS‑c administration ameliorated cardiac hypertrophy.

    In plain wordsIn neonatal mice with high-oxygen heart injury, MOTS‑c reduced heart enlargement.

    Peptide
    MOTS-c
    Outcome
    DecreaseCardiac hypertrophy
    Study

    mousen: not reported in source

    Hyperoxia-induced neonatal cardiac injury (85% O<sub>2</sub>)
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of MOTS-c markedly ameliorated these pathological changes and restored cardiac function.
    2 context sentences
    Summary · context
    We found that hyperoxia exposure in neonatal mice led to significant cardiac hypertrophy, fibrosis, and dysfunction, concomitant with decreased serum MOTS-c content.
    Summary · context
    Neonatal mice exposed hyperoxia (85% O2) were used to establish the hyperoxic cardiac injury model.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In hyperoxia-exposed neonatal mice, MOTS‑c administration ameliorated cardiac fibrosis.

    In plain wordsIn neonatal mice with high-oxygen heart injury, MOTS‑c reduced heart scarring.

    Peptide
    MOTS-c
    Outcome
    DecreaseCardiac fibrosis
    Study

    mousen: not reported in source

    Hyperoxia-induced neonatal cardiac injury (85% O<sub>2</sub>)
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of MOTS-c markedly ameliorated these pathological changes and restored cardiac function.
    2 context sentences
    Summary · context
    We found that hyperoxia exposure in neonatal mice led to significant cardiac hypertrophy, fibrosis, and dysfunction, concomitant with decreased serum MOTS-c content.
    Summary · context
    Neonatal mice exposed hyperoxia (85% O2) were used to establish the hyperoxic cardiac injury model.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In hyperoxia-exposed neonatal mice, MOTS‑c administration restored cardiac function.

    In plain wordsIn neonatal mice with high-oxygen heart injury, MOTS‑c restored heart function.

    Peptide
    MOTS-c
    Outcome
    IncreaseCardiac function
    Study

    mousen: not reported in source

    Hyperoxia-induced neonatal cardiac injury (85% O<sub>2</sub>)
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Administration of MOTS-c markedly ameliorated these pathological changes and restored cardiac function.
    2 context sentences
    Summary · context
    We found that hyperoxia exposure in neonatal mice led to significant cardiac hypertrophy, fibrosis, and dysfunction, concomitant with decreased serum MOTS-c content.
    Summary · context
    Neonatal mice exposed hyperoxia (85% O2) were used to establish the hyperoxic cardiac injury model.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In hyperoxia-exposed neonatal mice, MOTS‑c inhibited oxeiptosis, a ROS-specific cell death.

    In plain wordsIn neonatal mice with high-oxygen heart injury, MOTS‑c reduced a type of cell death linked to oxidative stress.

    Peptide
    MOTS-c
    Outcome
    DecreaseOxeiptosis in hyperoxic heart injury (in vivo)
    Study

    mousen: not reported in source

    Hyperoxia-induced neonatal cardiac injury (85% O<sub>2</sub>)
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro and in vivo experiments revealed that hyperoxia triggers oxidative stress and oxeiptosis via activating KEAP1-PGAM5-AIFM1 axis, and MOTS-c inhibited oxeiptosis.
    2 context sentences
    Summary · context
    Oxeiptosis is a ROS-specific programmed cell death.
    Summary · context
    Neonatal mice exposed hyperoxia (85% O2) were used to establish the hyperoxic cardiac injury model.
  5. 05AnimalAnimal study (in vivo)Mechanism

    MOTS‑c could potentially interact with KEAP1 and thereby maintain the KEAP1-PGAM5 interaction in hyperoxic cardiac injury.

    In plain wordsIn the hyperoxia models, MOTS‑c may bind KEAP1 and so keep the KEAP1-PGAM5 link in place.

    Peptide
    MOTS-c
    Outcome
    IncreaseKEAP1-PGAM5 interaction
    Study

    mousen: not reported in source

    Hyperoxia-induced neonatal cardiac injury (85% O<sub>2</sub>)
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, MOTS-c could potentially interact with KEAP1, thereby maintaining the KEAP1-PGAM5 interaction, and inhibiting the downstream nuclear translocation of AIFM1.
    1 context sentence
    Summary · context
    Neonatal mice exposed hyperoxia (85% O2) were used to establish the hyperoxic cardiac injury model.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In the hyperoxia models, MOTS‑c inhibited the downstream nuclear translocation of AIFM1.

    In plain wordsIn the hyperoxia models, MOTS‑c reduced the movement of AIFM1 into the cell nucleus.

    Peptide
    MOTS-c
    Outcome
    DecreaseAIFM1 nuclear translocation
    Study

    mousen: not reported in source

    Hyperoxia-induced neonatal cardiac injury (85% O<sub>2</sub>)
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, MOTS-c could potentially interact with KEAP1, thereby maintaining the KEAP1-PGAM5 interaction, and inhibiting the downstream nuclear translocation of AIFM1.
    1 context sentence
    Summary · context
    Neonatal mice exposed hyperoxia (85% O2) were used to establish the hyperoxic cardiac injury model.
  7. 07AnimalAnimal study (in vivo)Mechanism

    KEAP1 overexpression abrogated the protective effects of MOTS‑c in hyperoxia-induced cardiac injury.

    In plain wordsWhen KEAP1 was made more abundant, MOTS‑c no longer protected against high-oxygen heart injury in the models.

    Peptide
    MOTS-c
    Outcome
    No significant changeMOTS-c protection with KEAP1 overexpression
    Study

    mousen: not reported in source

    Hyperoxia-induced neonatal cardiac injury (85% O<sub>2</sub>)
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, KEAP1 overexpression abrogated the protective effects of MOTS-c, confirming KEAP1 as a critical target of MOTS-c in hyperoxia-induced cardiac injury.
    1 context sentence
    Summary · context
    Neonatal mice exposed hyperoxia (85% O2) were used to establish the hyperoxic cardiac injury model.
  8. 08LabIn vitro (cells)Mechanism

    In hyperoxia-exposed H9C2 cardiomyocytes, MOTS‑c inhibited oxeiptosis.

    In plain wordsIn cells from rat heart muscle under high oxygen, MOTS‑c reduced a type of cell death linked to oxidative stress.

    Peptide
    MOTS-c
    Outcome
    DecreaseOxeiptosis in hyperoxic cardiomyocytes (in vitro)
    Study

    ratn: not reported in source

    H9C2 cardiomyocytes under hyperoxia
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro and in vivo experiments revealed that hyperoxia triggers oxidative stress and oxeiptosis via activating KEAP1-PGAM5-AIFM1 axis, and MOTS-c inhibited oxeiptosis.
    1 context sentence
    Summary · context
    Additionally, the rat cardiomyocyte cell line H9C2 were subjected to hyperoxic conditions as an in vitro model.

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. 09AnimalEndogenous levelAnimal study (in vivo)Other

    In neonatal mice, hyperoxia exposure decreased the body's own serum MOTS‑c content.

    In plain wordsIn neonatal mice, high oxygen lowered the body's own MOTS‑c level in the blood.

    Peptide
    MOTS-c
    Outcome
    DecreaseSerum MOTS-c content under hyperoxia
    Study

    mousen: not reported in source

    Hyperoxia-induced neonatal cardiac injury (85% O<sub>2</sub>)
    Outcome group
    Mitochondrial function · Cardiovascular

    Source sentences

    Summary
    We found that hyperoxia exposure in neonatal mice led to significant cardiac hypertrophy, fibrosis, and dysfunction, concomitant with decreased serum MOTS-c content.
    1 context sentence
    Summary · context
    Neonatal mice exposed hyperoxia (85% O2) were used to establish the hyperoxic cardiac injury 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

    9 Oct 2026, 18:17 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

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