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

12 results

The role of FPR2-mediated ferroptosis in formyl peptide-induced acute lung injury against endothelial barrier damage and protective effect of the mitochondria-derived peptide MOTS-c.

Wen Z, Fan J, Zhan F, Li X, Li B, Lu P, Yao X, Shen Z, Liu Z, Wang C, Li X, Jin W and 4 more

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Zhang X, Qi Y, Wang X, Song M

International immunopharmacology24 Mar 2024Cited by 11 (Europe PMC)

PMID38527401 (opens in a new tab)DOI10.1016/j.intimp.2024.111911 (opens in a new tab)PepBankPUB-38527401
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: CC BY-NC-ND. Results still quote short attributed sentences.

Results from this study12

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In rats with fMLP-induced acute lung injury, MOTS‑c protected vascular endothelial barrier function.

    In plain wordsIn rats with lung injury, MOTS‑c protected the barrier that lines the blood vessels.

    Peptide
    MOTS-c
    Outcome
    IncreaseEndothelial barrier function (vascular)
    Study

    ratn: not reported in source

    fMLP-induced acute lung injury
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MOTS-c could protect the vascular endothelial barrier function by inhibiting ferroptosis and suppressing the expression of inflammatory and oxidative stress factors through Nrf2 and MAPK pathways, thereby alleviating fMLP-induced ALI.
    1 context sentence
    Summary · context
    We established a rat model of ALI and a human pulmonary microvascular endothelial cell (HPMVEC) model of ALI by treatment with fMLP.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In rats with fMLP-induced acute lung injury, MOTS‑c inhibited ferroptosis.

    In plain wordsIn rats with lung injury, MOTS‑c reduced a form of cell death called ferroptosis.

    Peptide
    MOTS-c
    Outcome
    DecreaseFerroptosis
    Study

    ratn: not reported in source

    fMLP-induced acute lung injury
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MOTS-c could protect the vascular endothelial barrier function by inhibiting ferroptosis and suppressing the expression of inflammatory and oxidative stress factors through Nrf2 and MAPK pathways, thereby alleviating fMLP-induced ALI.
    1 context sentence
    Summary · context
    We established a rat model of ALI and a human pulmonary microvascular endothelial cell (HPMVEC) model of ALI by treatment with fMLP.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In rats with fMLP-induced acute lung injury, MOTS‑c suppressed the expression of inflammatory factors.

    In plain wordsIn rats with lung injury, MOTS‑c lowered the levels of inflammation molecules.

    Peptide
    MOTS-c
    Outcome
    DecreaseInflammatory factor expression
    Study

    ratn: not reported in source

    fMLP-induced acute lung injury
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MOTS-c could protect the vascular endothelial barrier function by inhibiting ferroptosis and suppressing the expression of inflammatory and oxidative stress factors through Nrf2 and MAPK pathways, thereby alleviating fMLP-induced ALI.
    1 context sentence
    Summary · context
    We established a rat model of ALI and a human pulmonary microvascular endothelial cell (HPMVEC) model of ALI by treatment with fMLP.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In rats with fMLP-induced acute lung injury, MOTS‑c suppressed the expression of oxidative stress factors.

    In plain wordsIn rats with lung injury, MOTS‑c lowered oxidative stress molecules.

    Peptide
    MOTS-c
    Outcome
    DecreaseOxidative stress factor expression
    Study

    ratn: not reported in source

    fMLP-induced acute lung injury
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MOTS-c could protect the vascular endothelial barrier function by inhibiting ferroptosis and suppressing the expression of inflammatory and oxidative stress factors through Nrf2 and MAPK pathways, thereby alleviating fMLP-induced ALI.
    1 context sentence
    Summary · context
    We established a rat model of ALI and a human pulmonary microvascular endothelial cell (HPMVEC) model of ALI by treatment with fMLP.
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In rats, MOTS‑c alleviated acute lung injury induced by fMLP.

    In plain wordsIn rats, MOTS‑c reduced lung injury caused by a bacterial peptide.

    Peptide
    MOTS-c
    Outcome
    DecreasefMLP-induced acute lung injury
    Study

    ratn: not reported in source

    fMLP-induced acute lung injury
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MOTS-c could protect the vascular endothelial barrier function by inhibiting ferroptosis and suppressing the expression of inflammatory and oxidative stress factors through Nrf2 and MAPK pathways, thereby alleviating fMLP-induced ALI.
    1 context sentence
    Summary · context
    We established a rat model of ALI and a human pulmonary microvascular endothelial cell (HPMVEC) model of ALI by treatment with fMLP.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In rats with fMLP-induced acute lung injury, the protection by MOTS‑c worked through the Nrf2 and MAPK pathways.

    In plain wordsIn rats with lung injury, MOTS‑c acted through the Nrf2 and MAPK signal pathways.

    Peptide
    MOTS-c
    Outcome
    Not applicableInvolvement of Nrf2 and MAPK pathways
    Study

    ratn: not reported in source

    fMLP-induced acute lung injury
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MOTS-c could protect the vascular endothelial barrier function by inhibiting ferroptosis and suppressing the expression of inflammatory and oxidative stress factors through Nrf2 and MAPK pathways, thereby alleviating fMLP-induced ALI.
    1 context sentence
    Summary · context
    We established a rat model of ALI and a human pulmonary microvascular endothelial cell (HPMVEC) model of ALI by treatment with fMLP.
  7. 07LabIn vitro (cells)Efficacy outcome

    In human pulmonary microvascular endothelial cells treated with fMLP, MOTS‑c protected vascular endothelial barrier function.

    In plain wordsIn human lung blood-vessel cells in the lab, MOTS‑c protected the cell barrier.

    Peptide
    MOTS-c
    Outcome
    IncreaseEndothelial barrier function (vascular)
    Study

    humann: not reported in source

    HPMVEC treated with fMLP
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MOTS-c could protect the vascular endothelial barrier function by inhibiting ferroptosis and suppressing the expression of inflammatory and oxidative stress factors through Nrf2 and MAPK pathways, thereby alleviating fMLP-induced ALI.
    1 context sentence
    Summary · context
    We established a rat model of ALI and a human pulmonary microvascular endothelial cell (HPMVEC) model of ALI by treatment with fMLP.
  8. 08LabIn vitro (cells)Mechanism

    In human pulmonary microvascular endothelial cells treated with fMLP, MOTS‑c inhibited ferroptosis.

    In plain wordsIn human lung blood-vessel cells in the lab, MOTS‑c reduced ferroptosis, a form of cell death.

    Peptide
    MOTS-c
    Outcome
    DecreaseFerroptosis
    Study

    humann: not reported in source

    HPMVEC treated with fMLP
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MOTS-c could protect the vascular endothelial barrier function by inhibiting ferroptosis and suppressing the expression of inflammatory and oxidative stress factors through Nrf2 and MAPK pathways, thereby alleviating fMLP-induced ALI.
    1 context sentence
    Summary · context
    We established a rat model of ALI and a human pulmonary microvascular endothelial cell (HPMVEC) model of ALI by treatment with fMLP.
  9. 09LabIn vitro (cells)Mechanism

    In human pulmonary microvascular endothelial cells treated with fMLP, MOTS‑c suppressed the expression of inflammatory factors.

    In plain wordsIn human lung blood-vessel cells in the lab, MOTS‑c lowered inflammation molecules.

    Peptide
    MOTS-c
    Outcome
    DecreaseInflammatory factor expression
    Study

    humann: not reported in source

    HPMVEC treated with fMLP
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MOTS-c could protect the vascular endothelial barrier function by inhibiting ferroptosis and suppressing the expression of inflammatory and oxidative stress factors through Nrf2 and MAPK pathways, thereby alleviating fMLP-induced ALI.
    1 context sentence
    Summary · context
    We established a rat model of ALI and a human pulmonary microvascular endothelial cell (HPMVEC) model of ALI by treatment with fMLP.
  10. 10LabIn vitro (cells)Mechanism

    In human pulmonary microvascular endothelial cells treated with fMLP, MOTS‑c suppressed the expression of oxidative stress factors.

    In plain wordsIn human lung blood-vessel cells in the lab, MOTS‑c lowered oxidative stress molecules.

    Peptide
    MOTS-c
    Outcome
    DecreaseOxidative stress factor expression
    Study

    humann: not reported in source

    HPMVEC treated with fMLP
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MOTS-c could protect the vascular endothelial barrier function by inhibiting ferroptosis and suppressing the expression of inflammatory and oxidative stress factors through Nrf2 and MAPK pathways, thereby alleviating fMLP-induced ALI.
    1 context sentence
    Summary · context
    We established a rat model of ALI and a human pulmonary microvascular endothelial cell (HPMVEC) model of ALI by treatment with fMLP.
  11. 11LabIn vitro (cells)Efficacy outcome

    In human pulmonary microvascular endothelial cells, MOTS‑c alleviated injury induced by fMLP.

    In plain wordsIn human lung blood-vessel cells in the lab, MOTS‑c reduced damage caused by a bacterial peptide.

    Peptide
    MOTS-c
    Outcome
    DecreasefMLP-induced acute lung injury
    Study

    humann: not reported in source

    HPMVEC treated with fMLP
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MOTS-c could protect the vascular endothelial barrier function by inhibiting ferroptosis and suppressing the expression of inflammatory and oxidative stress factors through Nrf2 and MAPK pathways, thereby alleviating fMLP-induced ALI.
    1 context sentence
    Summary · context
    We established a rat model of ALI and a human pulmonary microvascular endothelial cell (HPMVEC) model of ALI by treatment with fMLP.
  12. 12LabIn vitro (cells)Mechanism

    In human pulmonary microvascular endothelial cells treated with fMLP, the protection by MOTS‑c worked through the Nrf2 and MAPK pathways.

    In plain wordsIn human lung blood-vessel cells in the lab, MOTS‑c acted through the Nrf2 and MAPK signal pathways.

    Peptide
    MOTS-c
    Outcome
    Not applicableInvolvement of Nrf2 and MAPK pathways
    Study

    humann: not reported in source

    HPMVEC treated with fMLP
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, MOTS-c could protect the vascular endothelial barrier function by inhibiting ferroptosis and suppressing the expression of inflammatory and oxidative stress factors through Nrf2 and MAPK pathways, thereby alleviating fMLP-induced ALI.
    1 context sentence
    Summary · context
    We established a rat model of ALI and a human pulmonary microvascular endothelial cell (HPMVEC) model of ALI by treatment with fMLP.

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

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