ReviewJournal of cardiovascular translational research2012
The extracellular matrix modulates fibroblast phenotype and function in the infarcted myocardium.
Review in Journal of cardiovascular translational research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed.
- Full-field analysis indicates late reperfusion therapy broadens and mechanically smooths the borderzone during post-infarction inflammation.Acta biomaterialia · 2026Article
- SASP-mediated cellular senescence following myocardial infarction: from spatiotemporal immune regulation to therapeutic strategies.Frontiers in immunology · 2026Review
- Cationic microbubble loading hSIRT3 and hTIMP3 optimize cardiac-targeted delivery and myocardial protection in the porcine MI/R model.Materials today. Bio · 2025Article
- Proteome Alterations in Cardiac Fibroblasts: Insights from Experimental Myocardial Infarction and Clinical Ischaemic Cardiomyopathy.International journal of molecular sciences · 2025Article
- Cancer associated fibroblasts in cancer development and therapy.Journal of hematology & oncology · 2025Review
- Endotrophin, a Key Marker and Driver for Fibroinflammatory Disease.Endocrine reviews · 2024Review
- Novel Therapies for the Treatment of Cardiac Fibrosis Following Myocardial Infarction.Biomedicines · 2022Review
- Canadian Contributions in Fibroblast Biology.Cells · 2022Review
- Review
- MBNL1 drives dynamic transitions between fibroblasts and myofibroblasts in cardiac wound healing.Cell stem cell · 2022Article
- Ginsenoside Rg2 alleviates myocardial fibrosis by regulating TGF-β1/Smad signalling pathway.Pharmaceutical biology · 2021Article
- Discoidin Domain Receptor 2 Regulates AT1R Expression in Angiotensin II-Stimulated Cardiac Fibroblasts via Fibronectin-Dependent Integrin-β1 Signaling.International journal of molecular sciences · 2021Article
- MicroRNA‑331 inhibits isoproterenol‑induced expression of profibrotic genes in cardiac myofibroblasts via the TGFβ/smad3 signaling pathway.Scientific reports · 2021Article
- Photoacoustic Imaging of Myocardial Infarction Region Using Non-Invasive Fibrin-Targeted Nanoparticles in a Rat Myocardial Ischemia-Reperfusion Model.International journal of nanomedicine · 2021Article
- Small molecule inhibitor of HSP47 prevents pro-fibrotic mechanisms of fibroblasts in vitro.Biochemical and biophysical research communications · 2020Article
- Regulators of cardiac fibroblast cell state.Matrix biology : journal of the International Society for Matrix Biology · 2020Review
- Immunotherapy for Infarcts:BioResearch open access · 2020Article
- Regulation of Myocardial Extracellular Matrix Dynamic Changes in Myocardial Infarction and Postinfarct Remodeling.Current cardiology reviews · 2020Review
- Isoproterenol Increases Left Atrial Fibrosis and Susceptibility to Atrial Fibrillation by Inducing Atrial Ischemic Infarction in Rats.Frontiers in pharmacology · 2020Article
- Biomechanical assessment of remote and postinfarction scar remodeling following myocardial infarction.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Cardiac fibroblasts are key cellular effectors of cardiac repair; their phenotype and function are modulated by interactions with extracellular matrix proteins. This review manuscript discusses the effects of the extracellular matrix on the inflammatory and reparative properties of fibroblasts in the infarcted myocardium. Early generation of matrix fragments in the infarct induces a pro-inflammatory and matrix-degrading fibroblast phenotype. Formation of a fibrin/fibronectin-rich provisional matrix serves as a conduit for migration of fibroblasts into the infarcted area. Induction of ED-A fibronectin and nonfibrillar collagens may contribute to myofibroblast transdifferentiation. Upregulation of matricellular proteins promotes transduction of growth factor and cytokine-mediated signals. As the scar matures, matrix cross-linking, clearance of matricellular proteins, and reduced growth factor signaling cause deactivation and apoptosis of reparative infarct fibroblasts. Understanding the effects of matrix components on infarct fibroblasts may guide the design of peptides that reproduce, or inhibit, specific matricellular functions, attenuating adverse remodeling.
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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.