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

5 results

Inhibition of TREM1 attenuates myocardial ischemia-reperfusion injury-induced cardiomyocyte pyroptosis by suppressing the activation of the NF-κB signaling pathway.

Xu X, Cai L, Dang X, Han J, Kou Y, Rong C, Kou J

PloS one9 Jan 2026Cited by 3 (Europe PMC)

PMID41511954 (opens in a new tab)PMCIDPMC12788684 (opens in a new tab)DOI10.1371/journal.pone.0340382 (opens in a new tab)PepBankPUB-41511954
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Summary

BackgroundTriggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of inflammatory responses and plays a critical role in the pathogenesis of various infectious diseases. Notably, emerging evidence suggests that TREM-1 is also involved in the development and progression of cardiovascular diseases, such as atherosclerosis and atrial fibrillation. However, its role in myocardial ischemia/reperfusion (I/R) injury remains unclear. This study aimed to investigate the role of TREM-1 in myocardial I/R injury and to explore the potential underlying molecular mechanisms.MethodsA hypoxia/reoxygenation (H/R) model was established using HL-1 cardiomyocytes subjected to 6 hours of hypoxia followed by 6 hours of reoxygenation. Pyroptosis levels were assessed by Hoechst-PI staining, lactate dehydrogenase (LDH) release assay, CCK-8 assay, and Western blot analysis. In vivo, a myocardial I/R injury model was established in C57BL/6 mice by subjecting them to 30 minutes of ischemia followed by 24 hours or 7 days of reperfusion. Evaluation was performed using TTC staining, Western blotting, echocardiography, histochemical staining, and immunohistochemistry.ResultsIn this study, we found that TREM-1 expression was significantly upregulated in both in vitro and in vivo models of myocardial ischemia-reperfusion injury (MIRI). Pharmacological inhibition of TREM-1 by LR12 effectively reduced the levels of cardiomyocyte pyroptosis and suppressed activation of the NF-κB signaling pathway. In addition, LR12 treatment alleviated myocardial inflammation and fibrosis and improved left ventricular function in mice.Intervention experiments with MCC950, a specific NLRP3 inhibitor, confirmed that NLRP3 inhibition could mimic the anti-pyroptotic effect of LR12 and reduce the expression of pyroptosis-related proteins. Immunofluorescence experiments further verified that inhibition of NF-κB decreased NLRP3 expression, clarifying the association between TREM-1 downstream signals and NLRP3. Long-term follow-up experiments showed that LR12 treatment significantly reduced the area of myocardial fibrosis at 7 days after reperfusion.ConclusionOur findings indicate that inhibition of TREM-1 alleviates cardiomyocyte pyroptosis during MIRI by suppressing activation of the NF-κB signaling pathway. Therefore, TREM-1 may represent a promising therapeutic target for the treatment of myocardial ischemia-reperfusion injury.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study5

5 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 myocardial ischemia-reperfusion injury, LR12 alleviated myocardial inflammation.

    In plain wordsIn mice, LR12 reduced myocardial inflammation.

    Peptide
    Nangibotide
    Outcome
    DecreaseMyocardial inflammation
    Study

    mousen: not reported in source

    Myocardial ischemia-reperfusion injury
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, LR12 treatment alleviated myocardial inflammation and fibrosis and improved left ventricular function in mice.
    1 context sentence
    Summary · context
    In vivo, a myocardial I/R injury model was established in C57BL/6 mice by subjecting them to 30 minutes of ischemia followed by 24 hours or 7 days of reperfusion.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice with myocardial ischemia-reperfusion injury, LR12 improved left ventricular function.

    In plain wordsIn mice, LR12 improved left ventricular function.

    Peptide
    Nangibotide
    Outcome
    IncreaseLeft ventricular function
    Study

    mousen: not reported in source

    Myocardial ischemia-reperfusion injury
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, LR12 treatment alleviated myocardial inflammation and fibrosis and improved left ventricular function in mice.
    1 context sentence
    Summary · context
    In vivo, a myocardial I/R injury model was established in C57BL/6 mice by subjecting them to 30 minutes of ischemia followed by 24 hours or 7 days of reperfusion.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mice, LR12 significantly reduced myocardial fibrosis area at 7 days after reperfusion.

    In plain wordsIn mice, LR12 reduced myocardial fibrosis area at 7 days after reperfusion.

    Peptide
    Nangibotide
    Outcome
    DecreaseMyocardial fibrosis area at follow-up
    Study

    mousen: not reported in source

    Myocardial ischemia-reperfusion injury
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Long-term follow-up experiments showed that LR12 treatment significantly reduced the area of myocardial fibrosis at 7 days after reperfusion.
    1 context sentence
    Summary · context
    In vivo, a myocardial I/R injury model was established in C57BL/6 mice by subjecting them to 30 minutes of ischemia followed by 24 hours or 7 days of reperfusion.
  4. 04AnimalOther designEfficacy outcome

    In myocardial ischemia-reperfusion models, LR12 reduced cardiomyocyte pyroptosis.

    In plain wordsIn experimental models, LR12 reduced cardiomyocyte pyroptosis.

    Peptide
    Nangibotide
    Outcome
    DecreaseCardiomyocyte pyroptosis
    Study

    n: not reported in source

    Myocardial ischemia-reperfusion models
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pharmacological inhibition of TREM-1 by LR12 effectively reduced the levels of cardiomyocyte pyroptosis and suppressed activation of the NF-κB signaling pathway.
  5. 05AnimalOther designMechanism

    In myocardial ischemia-reperfusion models, LR12 suppressed NF-κB pathway activation.

    In plain wordsIn experimental models, LR12 suppressed NF-κB pathway activation.

    Peptide
    Nangibotide
    Outcome
    DecreaseNF-κB pathway activation
    Study

    n: not reported in source

    Myocardial ischemia-reperfusion models
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pharmacological inhibition of TREM-1 by LR12 effectively reduced the levels of cardiomyocyte pyroptosis and suppressed activation of the NF-κB signaling pathway.

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

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