ArticleExperimental biology and medicine (Maywood, N.J.)2004
Inflammation and ischemia: macrophages activated by fibronectin fragments enhance the survival of injured cardiac myocytes.
Article in Experimental biology and medicine (Maywood, N.J.), 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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
31 citing papers in PubMed, 61 citations in OpenAlex.
- Full-field analysis indicates late reperfusion therapy broadens and mechanically smooths the borderzone during post-infarction inflammation.Acta biomaterialia · 2026Article
- Hydrogel-Delivered Recombinant Fibronectin DK1 Promotes Diabetic Wound Healing by Boosting Cellular Responses.Biomolecules · 2026Article
- Translational Extracellular Matrix Spray-Coating Approach for Large-Scale Bioactive Surface Functionalization and Tissue Repair.Advanced healthcare materials · 2025Article
- EDA Fibronectin Microarchitecture and YAP Translocation during Wound Closure.ACS biomaterials science & engineering · 2025Article
- Hyaluronan provokes inflammation but suppresses phagocytotic function in macrophages.Journal of molecular and cellular cardiology · 2025Article
- Macrophage-based therapeutic approaches for cardiovascular diseases.Basic research in cardiology · 2024Review
- Gut microbiota might mediate the benefits of high-fiber/acetate diet to cardiac hypertrophy mice.Journal of physiology and biochemistry · 2023Article
- Crosstalk Between Cardiac Cells and Macrophages Postmyocardial Infarction: Insights fromTissue engineering. Part B, Reviews · 2021Review
- Macrophage Activities in Myocardial Infarction and Heart Failure.Cardiology research and practice · 2020Review
- MMP-9/Gelatinase B Degrades Immune Complexes in Systemic Lupus Erythematosus.Frontiers in immunology · 2019Article
- Matrix metalloproteinase-12 as an endogenous resolution promoting factor following myocardial infarction.Pharmacological research · 2018Review
- Endothelial MMP-9 drives the inflammatory response in abdominal aortic aneurysm (AAA).American journal of translational research · 2017Article
- Stuck in the Middle: Fibronectin-Binding Proteins in Gram-Positive Bacteria.Frontiers in microbiology · 2016Review
- Emerging roles for macrophages in cardiac injury: cytoprotection, repair, and regeneration.The Journal of clinical investigation · 2015Article
- Heart regeneration with engineered myocardial tissue.Annual review of biomedical engineering · 2014Review
- Myofibroblasts and the extracellular matrix network in post-myocardial infarction cardiac remodeling.Pflugers Archiv : European journal of physiology · 2014Review
- Translating Koch's postulates to identify matrix metalloproteinase roles in postmyocardial infarction remodeling: cardiac metalloproteinase actions (CarMA) postulates.Circulation research · 2014Review
- Using plasma matrix metalloproteinase-9 and monocyte chemoattractant protein-1 to predict future cardiovascular events in subjects with carotid atherosclerosis.Atherosclerosis · 2014Article
- Matrix metalloproteinase-9: Many shades of function in cardiovascular disease.Physiology (Bethesda, Md.) · 2013Review
- Using proteomics to uncover extracellular matrix interactions during cardiac remodeling.Proteomics. Clinical applications · 2013Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Proteolytic enzymes, released early in the course of an inflammatory response, hydrolyze fibronectin, producing fragments of the parent molecule that alter monocyte phenotype and migratory behavior. Here we test the hypothesis that macrophages, stimulated by the dominant 110-120 kd fibronectin fragments (FNf), as are found in lymphatic fluid draining sites of cardiac ischemia-reperfusion injury, produce factors that promote the survival of injured parenchymal cells. Rat splenic macrophages stimulated in vitro with purified FNf produced soluble factors that protected hypoxic rat cardiac myocytes from death by apoptosis. Addition of blocking antibodies specific for tumor necrosis factor-alpha(TNF-alpha), fibroblast growth factor-1 (FGF-1), insulin-like growth factor I (IGF-I), and leukemia inhibitory factor (LIF) partly reduced the protection against apoptosis provided to hypoxic cardiac myocytes by cell-free culture supernatants from FNf-stimulated macrophages. Complete blockade of this protection was achieved by a combination of antibodies specific for FGF-1, IGF-I, and LIF. Stimulation of human monocyte-derived macrophages in vitro with FNf significantly increased their output of TNF-alpha, FGF-1, IGF-I, and LIF. These results suggest that tissue degradation products, released in the early hours of an inflammatory response, stimulate tissue-infiltrating macrophages to protect injured but still viable parenchymal cells from death by apoptosis.
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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.