ReviewJournal of molecular and cellular cardiology2010
Extracellular matrix turnover and signaling during cardiac remodeling following MI: causes and consequences.
Review in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 109 citations in OpenAlex.
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- Heart Scar-In-A-Dish: Tissue Culture Platform to Study Myocardial Injury and Mechanics In Vitro.Journal of biomechanical engineering · 2026Article
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- Shexiang Tongxin Dropping Pill Allieviates Heart Failure via Extracellula Matrix-Receptor Interaction Pathways Based on RNA-Seq Transcriptomics and Experimental Studies.Chinese journal of integrative medicine · 2023Article
- The cardiac wound healing response to myocardial infarction.WIREs mechanisms of disease · 2023Review
- Regulation of Collagen I and Collagen III in Tissue Injury and Regeneration.Cardiology and cardiovascular medicine · 2023Article
- Fibrillar Collagen Variants in Spontaneous Coronary Artery Dissection.JAMA cardiology · 2022Article
- Infarct in the Heart: What's MMP-9 Got to Do with It?Biomolecules · 2021Review
- Ubiquitin-specific protease 2 regulates Ang Ⅱ-induced cardiac fibroblasts activation by up-regulating cyclin D1 and stabilizing β-catenin in vitro.Journal of cellular and molecular medicine · 2021Article
- Biomechanics of infarcted left ventricle: a review of modelling.Biomedical engineering letters · 2020Review
- MiR-223-3p in Cardiovascular Diseases: A Biomarker and Potential Therapeutic Target.Frontiers in cardiovascular medicine · 2020Review
- Human peripheral blood‑derived exosomes for microRNA delivery.International journal of molecular medicine · 2019Article
- Cathepsin S degrades arresten and canstatin in infarcted area after myocardial infarction in rats.The Journal of veterinary medical science · 2019Article
- MiR-144-3p Enhances Cardiac Fibrosis After Myocardial Infarction by TargetingFrontiers in cell and developmental biology · 2019Article
- Proteomic analysis of the cardiac extracellular matrix: clinical research applications.Expert review of proteomics · 2018Review
- Flavonoid Extract from Propolis Inhibits Cardiac Fibrosis Triggered by Myocardial Infarction through Upregulation of SIRT1.Evidence-based complementary and alternative medicine : eCAM · 2018Article
- Proteomic footprint of myocardial ischemia/reperfusion injury: Longitudinal study of the at-risk and remote regions in the pig model.Scientific reports · 2017Article
- Astragaloside attenuates myocardial injury in a rat model of acute myocardial infarction by upregulating hypoxia inducible factor‑1α and Notch1/Jagged1 signaling.Molecular medicine reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The concept that extracellular matrix (ECM) turnover occurs during cardiac remodeling is a well-accepted paradigm. To date, a multitude of studies document that remodeling is accompanied by increases in the synthesis and deposition of ECM components as well as increases in extracellular proteases, especially matrix metalloproteinases (MMPs), which break down ECM components. Further, soluble ECM fragments generated from enzymatic action serve to stimulate cell behavior and have been proposed as candidate plasma biomarkers of cardiac remodeling. This review briefly summarizes our current knowledge base on cardiac ECM turnover following myocardial infarction (MI), but more importantly extends discussion by defining avenues that remain to be explored to drive the ECM remodeling field forward. Specifically, this review will discuss cause and effect roles for the ECM changes observed following MI and the potential role of the ECM changes that may serve as trigger points to regulate remodeling. While the pattern of remodeling following MI is qualitatively similar but quantitatively different from various types of injury, the basic theme in remodeling is repeated. Therefore, while we use the MI model as the prototype injury model, the themes discussed here are also relevant to cardiac remodeling due to other types of injury.
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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.