ArticleESC heart failure2015
Pharmacological inhibition of the triggering receptor expressed on myeloid cells-1 limits reperfusion injury in a porcine model of myocardial infarction.
Article in ESC heart failure, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- A first-in-man safety and pharmacokinetics study of nangibotide, a new modulator of innate immune response through TREM-1 receptor inhibition.British journal of clinical pharmacology · 2018Trial
- Trem1 exacerbates myocardial infarction-induced heart failure by inactivating the Rap1 pathway.Journal of cardiothoracic surgery · 2026Article
- TREM-1 inhibitor specificity and timing of treatment initiation can impact its therapeutic efficacy in cancer and inflammatory disease.Frontiers in oncology · 2025Article
- Cross-talk between cardiac lymphatics and immune cells regulates inflammatory response and cardiac recovery after myocardial infarction.Frontiers in immunology · 2025Review
- Inhibiting triggering receptor expressed on myeloid cells 1 signaling to ameliorate skin fibrosis.JCI insight · 2024Article
- TREM-1 and TREM-2 as therapeutic targets: clinical challenges and perspectives.Frontiers in immunology · 2024Article
- Evaluation of the efficacy and safety of TREM-1 inhibition with nangibotide in patients with COVID-19 receiving respiratory support: the ESSENTIAL randomised, double-blind trial.EClinicalMedicine · 2023Article
- The role of endogenous Smad7 in regulating macrophage phenotype following myocardial infarction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Soluble triggering receptor expressed on myeloid cells-1 is a marker of organ injuries in cardiogenic shock: results from the CardShock Study.Clinical research in cardiology : official journal of the German Cardiac Society · 2022Article
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- Novel ligands and modulators of triggering receptor expressed on myeloid cells receptor family: 2015-2020 updates.Expert opinion on therapeutic patents · 2021Review
- Triggering Receptor Expressed on Myeloid Cells-1 Inhibitor Targeted to Endothelium Decreases Cell Activation.Frontiers in immunology · 2019Article
- TREM-1; Is It a Pivotal Target for Cardiovascular Diseases?Journal of cardiovascular development and disease · 2018Review
- Pharmacological inhibition of the triggering receptor expressed on myeloid cells-1 limits reperfusion injury in a porcine model of myocardial infarction.ESC heart failure · 2015Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsLimitation of ischemia/reperfusion injury is a major therapeutic target after acute myocardial infarction (AMI). Toll-like receptors are implicated in the inflammatory response that occurs during reperfusion. The triggering receptor expressed on myeloid cells (TREM)-1 acts as an amplifier of the immune response triggered by toll-like receptor engagement. We hypothesized that administration of a TREM-1 inhibitory peptide (LR12) could limit reperfusion injury in a porcine model of AMI. METHODS AND
resultsAMI was induced in 15 adult minipigs by a closed-chest coronary artery occlusion-reperfusion technique. Animals were randomized to receive LR12 or vehicle before reperfusion (LR12 n = 7, vehicle n = 8), and were monitored during 18 h. AMI altered hemodynamics and cardiac function, as illustrated by a drop of mean arterial pressure, cardiac index, cardiac power index, ejection fraction, and real-time pressure-volume loop-derived parameters. TREM-1 inhibition by LR12 significantly improved these dysfunctions (P < 0.03) and limited infarct size, as assessed by lower creatine phosphokinase and troponin I concentrations (P < 0.005). Pulmonary, renal, and hepatic impairments occurred after AMI and were attenuated by LR12 administration as assessed by a better PaO
conclusionInhibition of the TREM-1 pathway by a synthetic peptide limited myocardial reperfusion injury in a clinically relevant porcine model of AMI.
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