ReviewJournal of cardiovascular translational research2012
Extracellular matrix and fibroblast communication following myocardial infarction.
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 46 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 81 citations in OpenAlex.
- Cardiac fibrosis: mechanistic insights and translational advances.Molecular biomedicine · 2026Review
- Post-MI Remodeling Mechanics of Left Ventricle: Microstructure-Informed Models, Identifiability, and Uncertainty for Patient-Specific Prediction.Bioengineering (Basel, Switzerland) · 2026Review
- Forces that shape the transcriptome: Linking cellular mechanosensing to mRNA splicing.The Journal of biological chemistry · 2026Review
- A Vaccine Against Fibroblast Activation Protein Improves Murine Cardiac Fibrosis by Preventing the Accumulation of Myofibroblasts.Circulation research · 2025Article
- Metalloproteinases (MMPs) in hypertensive disorders: role, function, pharmacology, and potential strategies to mitigate pathophysiological changes.Frontiers in pharmacology · 2025Review
- Immune in myocardial ischemia/reperfusion injury: potential mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
- The Contributions of Thrombospondin-1 to Epilepsy Formation.Neuroscience bulletin · 2024Review
- Cardiac Fibroblast Activation Induced by Oxygen-Glucose Deprivation Depends on the HIF-1α/miR-212-5p/KLF4 Pathway.Journal of cardiovascular translational research · 2023Article
- A Pharmacological Review of Tanshinones, Naturally Occurring Monomers fromOxidative medicine and cellular longevity · 2023Review
- Identification of Hub Genes in the Remodeling of Non-Infarcted Myocardium Following Acute Myocardial Infarction.Journal of cardiovascular development and disease · 2022Article
- Glutamine uptake and catabolism is required for myofibroblast formation and persistence.Journal of molecular and cellular cardiology · 2022Article
- Sex differences in cardiac remodeling post myocardial infarction with acute cigarette smoking.Biology of sex differences · 2022Article
- Emerging roles of circRNAs in the pathological process of myocardial infarction.Molecular therapy. Nucleic acids · 2021Review
- Extrinsically Conductive Nanomaterials for Cardiac Tissue Engineering Applications.Micromachines · 2021Review
- Tanshinone IIA Improves Ventricular Remodeling following Cardiac Infarction by Regulating miR-205-3p.Disease markers · 2021Article
- Cardiac fibroblast activation during myocardial infarction wound healing: Fibroblast polarization after MI.Matrix biology : journal of the International Society for Matrix Biology · 2020Review
- Myofibroblasts and Fibrosis: Mitochondrial and Metabolic Control of Cellular Differentiation.Circulation research · 2020Review
- Regulation of Myocardial Extracellular Matrix Dynamic Changes in Myocardial Infarction and Postinfarct Remodeling.Current cardiology reviews · 2020Review
- Transient Receptor Potential Ankyrin Type-1 Channels as a Potential Target for the Treatment of Cardiovascular Diseases.Frontiers in physiology · 2020Review
- Understanding cardiac extracellular matrix remodeling to develop biomarkers of myocardial infarction outcomes.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The extracellular matrix (ECM) provides structural support by serving as a scaffold for cells, and as such the ECM maintains normal tissue homeostasis and mediates the repair response following injury. In response to myocardial infarction (MI), ECM expression is generally upregulated in the left ventricle (LV), which regulates LV remodeling by modulating scar formation. The ECM directly affects scar formation by regulating growth factor release and cell adhesion and indirectly affects scar formation by regulating the inflammatory, angiogenic, and fibroblast responses. This review summarizes the current literature on ECM expression patterns and fibroblast mechanisms in the myocardium, focusing on the ECM response to MI. In addition, we discuss future research areas that are needed to better understand the molecular mechanisms of ECM action, both in general and as a means to optimize infarct healing.
Indexed as
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What OpenQuestion holds
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.