ArticleJournal of molecular and cellular cardiology2016
N-terminal fragment of cardiac myosin binding protein-C triggers pro-inflammatory responses in vitro.
Article in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Identification and validation of ANXA3 and SOCS3 as biomarkers for acute myocardial infarction related to sphingolipid metabolism.Hereditas · 2025Article
- Crosstalk between myocardial autophagy and sterile inflammation in the development of heart failure.Autophagy reports · 2024Review
- Chronic Benzene Exposure Aggravates Pressure Overload-Induced Cardiac Dysfunction.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Amino terminus of cardiac myosin binding protein-C regulates cardiac contractility.Journal of molecular and cellular cardiology · 2021Article
- Article
- Genetic, clinical, molecular, and pathogenic aspects of the South Asian-specific polymorphic MYBPC3Biophysical reviews · 2020Review
- When Innate Immunity Meets Angiogenesis-The Role of Toll-Like Receptors in Endothelial Cells and Pulmonary Hypertension.Frontiers in medicine · 2020Review
- The Dynamic Interplay Between Cardiac Inflammation and Fibrosis.Frontiers in physiology · 2020Review
- Non-Invasive Approach for Evaluation of Pulmonary Hypertension Using Extracellular Vesicle-Associated Small Non-Coding RNA.Biomolecules · 2019Article
- Cardiac Myosin-Binding Protein C-From Bench to Improved Diagnosis of Acute Myocardial Infarction.Cardiovascular drugs and therapy · 2019Review
- Ablation of the calpain-targeted site in cardiac myosin binding protein-C is cardioprotective during ischemia-reperfusion injury.Journal of molecular and cellular cardiology · 2019Article
- Danger-Associated Molecular Patterns Derived From the Extracellular Matrix Provide Temporal Control of Innate Immunity.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018Review
- Cell biological mechanisms in regulation of the post-infarction inflammatory response.Current opinion in physiology · 2018Article
- Role of the immune system in cardiac tissue damage and repair following myocardial infarction.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Review
- Simultaneous Isolation of High Quality Cardiomyocytes, Endothelial Cells, and Fibroblasts from an Adult Rat Heart.Journal of visualized experiments : JoVE · 2017Article
- Quantifying the Release of Biomarkers of Myocardial Necrosis from Cardiac Myocytes and Intact Myocardium.Clinical chemistry · 2017Article
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Myocardial infarction (MI) leads to loss and degradation of contractile cardiac tissue followed by sterile inflammation of the myocardium through activation and recruitment of innate and adaptive cells of the immune system. Recently, it was shown that cardiac myosin binding protein-C (cMyBP-C), a protein of the cardiac sarcomere, is degraded following MI, releasing a predominant N-terminal 40-kDa fragment (C0C1f) into myocardial tissue and the systemic circulation. We hypothesized that early release of C0C1f contributes to the initiation of inflammation and plays a key role in recruitment and activation of immune cells. Therefore, we investigated the role of C0C1f on macrophage/monocyte activation using both mouse bone marrow-derived macrophages and human monocytes. Here we demonstrate that C0C1f leads to macrophage/monocyte activation in vitro. Furthermore, C0C1f induces strong upregulation of pro-inflammatory cytokines (interleukin-6 (IL-6), tumor necrosis factor α (TNFα), and interleukin-1β (IL-1β)) in cultured murine macrophages and human monocytes, resulting in a pro-inflammatory phenotype. We identified the toll-like receptor 4 (TLR4), toll-like receptor 2 (TLR2), and Advanced Glycosylation End Product-Specific Receptor (RAGE) as potential receptors for C0C1f whose activation leads to mobilization of the NFκB signaling pathway, a central mediator of the pro-inflammatory signaling cascade. Thus, C0C1f appears to be a key player in the initiation of inflammatory processes and might also play an important role upon MI.
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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.