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Study · Not a test of the peptide alone · 2015

8 results

TREM-1 Mediates Inflammatory Injury and Cardiac Remodeling Following Myocardial Infarction.

Boufenzer A, Lemarié J, Simon T, Derive M, Bouazza Y, Tran N, Maskali F, Groubatch F, Bonnin P, Bastien C, Bruneval P, Marie PY and 5 more

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Cohen R, Danchin N, Silvestre JS, Ait-Oufella H, Gibot S

Circulation research3 Apr 2015Cited by 119 (Europe PMC)

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 study8

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone8

In this study, Nangibotide 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 Nangibotide.

  1. 01AnimalNot a test of Nangibotide aloneAnimal study (in vivo)Efficacy outcome

    In mice with infarction, genetic or LR12-mediated TREM-1 inhibition reduced myocardial inflammation.

    In plain wordsIn mice with infarction, genetic or LR12-mediated TREM-1 inhibition reduced heart inflammation.

    Outcome
    DecreaseMyocardial inflammation
    Study

    micen: not reported in source

    myocardial infarction
    Outcome group
    Inflammation markers · Cardiovascular

    Source sentences

    Summary
    Trem-1 genetic invalidation or pharmacological inhibition using a synthetic peptide (LR12) dampens myocardial inflammation, limits neutrophils recruitment and monocyte chemoattractant protein-1 production, thus reducing classical monocytes mobilization to the heart.

    In this study, Nangibotide 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 Nangibotide.

  2. 02AnimalNot a test of Nangibotide aloneAnimal study (in vivo)Mechanism

    In mice with infarction, genetic or LR12-mediated TREM-1 inhibition limited neutrophil recruitment.

    In plain wordsIn mice with infarction, genetic or LR12-mediated TREM-1 inhibition limited neutrophil recruitment.

    Outcome
    DecreaseNeutrophil recruitment
    Study

    micen: not reported in source

    myocardial infarction
    Outcome group
    Immune response · Cardiovascular

    Source sentences

    Summary
    Trem-1 genetic invalidation or pharmacological inhibition using a synthetic peptide (LR12) dampens myocardial inflammation, limits neutrophils recruitment and monocyte chemoattractant protein-1 production, thus reducing classical monocytes mobilization to the heart.

    In this study, Nangibotide 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 Nangibotide.

  3. 03AnimalNot a test of Nangibotide aloneAnimal study (in vivo)Mechanism

    In mice with infarction, genetic or LR12-mediated TREM-1 inhibition limited monocyte chemoattractant protein-1 production.

    In plain wordsIn mice with infarction, genetic or LR12-mediated TREM-1 inhibition limited monocyte chemoattractant protein-1 production.

    Outcome
    DecreaseMonocyte chemoattractant protein-1 production
    Study

    micen: not reported in source

    myocardial infarction
    Outcome group
    Inflammation markers · Cardiovascular

    Source sentences

    Summary
    Trem-1 genetic invalidation or pharmacological inhibition using a synthetic peptide (LR12) dampens myocardial inflammation, limits neutrophils recruitment and monocyte chemoattractant protein-1 production, thus reducing classical monocytes mobilization to the heart.

    In this study, Nangibotide 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 Nangibotide.

  4. 04AnimalNot a test of Nangibotide aloneAnimal study (in vivo)Mechanism

    In mice with infarction, genetic or LR12-mediated TREM-1 inhibition reduced classical monocyte mobilization to the heart.

    In plain wordsIn mice with infarction, genetic or LR12-mediated TREM-1 inhibition reduced classical monocyte movement to the heart.

    Outcome
    DecreaseClassical monocyte mobilization
    Study

    micen: not reported in source

    myocardial infarction
    Outcome group
    Immune response · Cardiovascular

    Source sentences

    Summary
    Trem-1 genetic invalidation or pharmacological inhibition using a synthetic peptide (LR12) dampens myocardial inflammation, limits neutrophils recruitment and monocyte chemoattractant protein-1 production, thus reducing classical monocytes mobilization to the heart.

    In this study, Nangibotide 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 Nangibotide.

  5. 05AnimalNot a test of Nangibotide aloneAnimal study (in vivo)Efficacy outcome

    In mice with infarction, genetic or LR12-mediated TREM-1 inhibition improved left ventricular function.

    In plain wordsIn mice with infarction, genetic or LR12-mediated TREM-1 inhibition improved left ventricular function.

    Outcome
    IncreaseLeft ventricular function
    Study

    micen: not reported in source

    myocardial infarction
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    It also improves left ventricular function and survival in mice (n=20-22 per group).
    1 context sentence
    Summary · context
    Trem-1 genetic invalidation or pharmacological inhibition using a synthetic peptide (LR12) dampens myocardial inflammation, limits neutrophils recruitment and monocyte chemoattractant protein-1 production, thus reducing classical monocytes mobilization to the heart.

    In this study, Nangibotide 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 Nangibotide.

  6. 06AnimalNot a test of Nangibotide aloneAnimal study (in vivo)Efficacy outcome

    In mice with infarction, genetic or LR12-mediated TREM-1 inhibition improved survival.

    In plain wordsIn mice with infarction, genetic or LR12-mediated TREM-1 inhibition improved survival.

    Outcome
    IncreaseSurvival
    Study

    micen: not reported in source

    myocardial infarction
    Outcome group
    Mortality · Whole body

    Source sentences

    Summary
    It also improves left ventricular function and survival in mice (n=20-22 per group).
    1 context sentence
    Summary · context
    Trem-1 genetic invalidation or pharmacological inhibition using a synthetic peptide (LR12) dampens myocardial inflammation, limits neutrophils recruitment and monocyte chemoattractant protein-1 production, thus reducing classical monocytes mobilization to the heart.

    In this study, Nangibotide 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 Nangibotide.

  7. 07AnimalNot a test of Nangibotide aloneAnimal study (in vivo)Efficacy outcome

    In mice with permanent or transient myocardial ischemia, TREM-1 blockade improved cardiac function, with uncertain LR12-specific attribution.

    In plain wordsIn mice with heart ischemia, TREM-1 blockade improved heart function, with uncertain LR12-specific attribution.

    Outcome
    IncreaseCardiac function during permanent and transient ischemia
    Study

    micen: not reported in source

    myocardial infarction
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    During both permanent and transient myocardial ischemia, Trem-1 blockade also ameliorates cardiac function and limits ventricular remodeling as assessed by fluorodeoxyglucose-positron emission tomographic imaging and conductance catheter studies (n=9-18 per group).
    1 context sentence
    Summary · context
    Trem-1 genetic invalidation or pharmacological inhibition using a synthetic peptide (LR12) dampens myocardial inflammation, limits neutrophils recruitment and monocyte chemoattractant protein-1 production, thus reducing classical monocytes mobilization to the heart.

    In this study, Nangibotide 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 Nangibotide.

  8. 08AnimalNot a test of Nangibotide aloneAnimal study (in vivo)Efficacy outcome

    In mice with permanent or transient myocardial ischemia, TREM-1 blockade limited ventricular remodeling, with uncertain LR12-specific attribution.

    In plain wordsIn mice with heart ischemia, TREM-1 blockade limited ventricular remodeling, with uncertain LR12-specific attribution.

    Outcome
    DecreaseVentricular remodeling
    Study

    micen: not reported in source

    myocardial infarction
    Outcome group
    Heart function · Cardiovascular

    Source sentences

    Summary
    During both permanent and transient myocardial ischemia, Trem-1 blockade also ameliorates cardiac function and limits ventricular remodeling as assessed by fluorodeoxyglucose-positron emission tomographic imaging and conductance catheter studies (n=9-18 per group).
    1 context sentence
    Summary · context
    Trem-1 genetic invalidation or pharmacological inhibition using a synthetic peptide (LR12) dampens myocardial inflammation, limits neutrophils recruitment and monocyte chemoattractant protein-1 production, thus reducing classical monocytes mobilization to the heart.

    In this study, Nangibotide 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 Nangibotide.

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

    27 Oct 2026, 18:20 UTC

    Study results updated

  2. Version 1

    27 Oct 2026, 16:32 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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