ArticleCritical care (London, England)2008
Fibrinogen decreases cardiomyocyte contractility through an ICAM-1-dependent mechanism.
Article in Critical care (London, England), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 31 citations in OpenAlex.
- Fibrinogen as a Molecular Bridge Linking SARS-CoV‑2 Immune Evasion and Endothelial Access?ACS pharmacology & translational science · 2026Article
- Targeted Treatment of Myocardial Infarction by Macrophage Membrane Coated with Resveratrol Nanoparticles.ACS omega · 2024Article
- Neoplastic ICAM-1 protects lung carcinoma from apoptosis through ligation of fibrinogen.Cell death & disease · 2024Article
- Effects of Three-Month Feeding High Fat Diets with Different Fatty Acid Composition on Myocardial Proteome in Mice.Nutrients · 2021Article
- A multiplex analysis of sepsis mediators during human septic shock: a preliminary study on myocardial depression and organ failures.Annals of intensive care · 2019Article
- Frequency Dependence of Petechial Hemorrhage and Cardiomyocyte Injury Induced during Myocardial Contrast Echocardiography.Ultrasound in medicine & biology · 2016Article
- Aging and the intramyocardial inflammatory response.Critical care (London, England) · 2014Article
- Deeper understanding of mechanisms contributing to sepsis-induced myocardial dysfunction.Critical care (London, England) · 2014Article
- Temporal and spatial expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases following myocardial infarction.Cardiovascular therapeutics · 2012Review
- Quercetin reduces inflammatory responses in LPS-stimulated cardiomyoblasts.Oxidative medicine and cellular longevity · 2012Article
- Article
- Fibrinogen-induced endothelin-1 production from endothelial cells.American journal of physiology. Cell physiology · 2009Article
- The malignant social network: cell-cell adhesion and communication in cancer stem cells.Cell adhesion & migrationReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionCardiomyocytes exposed to inflammatory processes express intracellular adhesion molecule-1 (ICAM-1). We investigated whether fibrinogen and fibrinogen degradation products, including D-dimer, could alter cardiomyocyte contractile function through interaction with ICAM-1 found on inflamed cardiomyocytes.
methodsIn vivo, rats were injected with endotoxin to model systemic inflammation, whereas isolated rat cardiomyocytes were treated with tumor necrosis factor-alpha to model the inflammatory environment seen following exposure to bacterial products such as lipopolysaccharide.
resultsIn vivo, endotoxin administration profoundly decreased cardiac contractile function associated with a large increase in intracardiac ICAM-1 and perivascular fibrinogen. Confocal microscopy with double-staining of isolated rat cardiomyocytes demonstrated colocalization of ICAM-1 and fibrinogen. This interaction was disrupted through pre-treatment of the cells with an ICAM-1-blocking antibody. Functionally, isolated rat cardiomyocyte preparations exhibited decreased fractional shortening when incubated with fibrinogen, and through the use of synthetic peptides, we determined that residues 117-133 of the fibrinogen gamma chain are responsible for this interaction with ICAM-1. Despite having crosslinked gamma chains, D-dimer retained the ability to decrease cardiomyocyte contractility.
conclusionSite 117-133 of the fibrinogen gamma chain is able to depress cardiomyocyte contractility through binding ICAM-1.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.