ArticleEMBO molecular medicine2014
S100A1 is released from ischemic cardiomyocytes and signals myocardial damage via Toll-like receptor 4.
Article in EMBO molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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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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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
42 citing papers in PubMed, 84 citations in OpenAlex.
- Neutrophil-Specific Biomarker S100A2 Mediates Diabetic Foot Ulcer Through IL-17 Signaling Pathway and Potential Therapeutics.Journal of inflammation research · 2026Article
- Damage-associated molecular patterns (DAMPs) in diseases: implications for therapy.Molecular biomedicine · 2025Review
- Advances in S100 protein family for gynecological malignancies.Discover oncology · 2025Review
- Macrophage Membrane-Coated Nanocarriers in Myocardial Infarction: A Paradigm Shift in Targeted Cardiac Therapy.International journal of nanomedicine · 2025Review
- Mechanical regulation of macrophage metabolism by allograft inflammatory factor 1 leads to adverse remodeling after cardiac injury.Nature cardiovascular research · 2025Article
- Role of the Receptor for Advanced Glycation End Products (RAGE) and Its Ligands in Inflammatory Responses.Biomolecules · 2024Review
- Calcium signaling in mitochondrial intermembrane space.Biochemical Society transactions · 2024Review
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities.Circulation research · 2024Review
- Proinflammatory cytokines driving cardiotoxicity in COVID-19.Cardiovascular research · 2024Article
- Mechanistic target of rapamycin in regulating macrophage function in inflammatory cardiovascular diseases.Journal of molecular and cellular cardiology · 2024Review
- S100A1 expression is increased in spinal cord injury and promotes inflammation, oxidative stress and apoptosis of PC12 cells induced by LPS via ERK signaling.Molecular medicine reports · 2023Article
- Observational
- Macrophages in myocardial infarction.American journal of physiology. Cell physiology · 2022Review
- Article
- Repurposing Multiple-Molecule Drugs for COVID-19-Associated Acute Respiratory Distress Syndrome and Non-Viral Acute Respiratory Distress Syndrome via a Systems Biology Approach and a DNN-DTI Model Based on Five Drug Design Specifications.International journal of molecular sciences · 2022Article
- Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022Review
- IL-1 Mediates Tissue-Specific Inflammation and Severe Respiratory Failure in COVID-19.Journal of innate immunity · 2022Article
- Hypoxia-inducible factors individually facilitate inflammatory myeloid metabolism and inefficient cardiac repair.The Journal of experimental medicine · 2021Article
- S100A gene family: immune-related prognostic biomarkers and therapeutic targets for low-grade glioma.Aging · 2021Article
- Mechanistic Insight Into the Regulation of Immune-Related Genes Expression in Autism Spectrum Disorder.Frontiers in molecular biosciences · 2021Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 3 countries.
Funding
Abstract
Members of the S100 protein family have been reported to function as endogenous danger signals (alarmins) playing an active role in tissue inflammation and repair when released from necrotic cells. Here, we investigated the role of S100A1, the S100 isoform with highest abundance in cardiomyocytes, when released from damaged cardiomyocytes during myocardial infarction (MI). Patients with acute MI showed significantly increased S100A1 serum levels. Experimental MI in mice induced comparable S100A1 release. S100A1 internalization was observed in cardiac fibroblasts (CFs) adjacent to damaged cardiomyocytes. In vitro analyses revealed exclusive S100A1 endocytosis by CFs, followed by Toll-like receptor 4 (TLR4)-dependent activation of MAP kinases and NF-κB. CFs exposed to S100A1 assumed an immunomodulatory and anti-fibrotic phenotype characterized i.e. by enhanced intercellular adhesion molecule-1 (ICAM1) and decreased collagen levels. In mice, intracardiac S100A1 injection recapitulated these transcriptional changes. Moreover, antibody-mediated neutralization of S100A1 enlarged infarct size and worsened left ventricular functional performance post-MI. Our study demonstrates alarmin properties for S100A1 from necrotic cardiomyocytes. However, the potentially beneficial role of extracellular S100A1 in MI-related inflammation and repair warrants further investigation.
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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.