ReviewJournal of molecular and cellular cardiology2016
Matrix metalloproteinases as input and output signals for post-myocardial infarction remodeling.
Review in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.
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
68 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Guidelines for experimental models of myocardial ischemia and infarction.American journal of physiology. Heart and circulatory physiology · 2018Guideline
- Functional Significance of Cardiac Rehabilitation-Regulated Expression of Circulating MicroRNA-423-5p in Hypertensive Patients with Heart Failure with a Moderately Reduced Ejection Fraction.Anatolian journal of cardiology · 2022Trial
- Trial
- MMP-9 Gene Ablation Preserves Ejection Fraction During "Single-Hit" Model of HFrEF.Biochemical genetics · 2026Article
- Myocardial Matrix Metalloproteinase 3 Protein Expression in Ischemic Heart Failure.International journal of molecular sciences · 2026Article
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- Endothelial-to-Mesenchymal Transition in Post-Myocardial Infarction Fibrosis: A Maladaptive but Targetable Pathway.EJIFCC · 2026Review
- Early Post-STEMI Cardiac Rehabilitation in the CSC-Infarct Program: Real-World Safety and Effectiveness of Individualized Training Protocols.Journal of clinical medicine · 2026Article
- NF-Frontiers in cardiovascular medicine · 2026Review
- Review
- Mapping the knowledge of omics in myocardial infarction: A scientometric analysis in R Studio, VOSviewer, Citespace, and SciMAT.Medicine · 2025Article
- Immunometabolism in the Aging Heart.Journal of the American Heart Association · 2025Review
- Retinol-binding protein 4 in skeletal and cardiac muscle: molecular mechanisms, clinical implications, and future perspectives.Frontiers in cell and developmental biology · 2025Review
- Therapeutic potential of human umbilical cord mesenchymal stem cell-derived exosomes in myocardial infarction: from molecular mechanisms to clinical translation-an update.Frontiers in pharmacology · 2025Review
- A Need to Preserve Ejection Fraction during Heart Failure.International journal of molecular sciences · 2024Review
- Article
- TFRC in cardiomyocytes promotes macrophage infiltration and activation during the process of heart failure through regulating Ccl2 expression mediated by hypoxia inducible factor-1α.Immunity, inflammation and disease · 2023Article
- IGF2BP3 promotes adult myocardial regeneration by stabilizing MMP3 mRNA through interaction with m6A modification.Cell death discovery · 2023Article
- Left Ventricular Hypertrophy and Ventricular Tachyarrhythmia: The Role of Biomarkers.International journal of molecular sciences · 2023Review
- Matrix Metalloproteinase-Targeted SPECT/CT Imaging for Evaluation of Therapeutic Hydrogels for the Early Modulation of Post-Infarct Myocardial Remodeling.Journal of cardiovascular translational research · 2023Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Despite current optimal therapeutic regimens, approximately one in four patients diagnosed with myocardial infarction (MI) will go on to develop congestive heart failure, and heart failure has a high five-year mortality rate of 50%. Elucidating mechanisms whereby heart failure develops post-MI, therefore, is highly needed. Matrix metalloproteinases (MMPs) are key enzymes involved in post-MI remodeling of the left ventricle (LV). While MMPs process cytokine and extracellular matrix (ECM) substrates to regulate the inflammatory and fibrotic components of the wound healing response to MI, MMPs also serve as upstream signaling initiators with direct actions on cell signaling cascades. In this review, we summarize the current literature regarding MMP roles in post-MI LV remodeling. We also identify the current knowledge gaps and provide templates for experiments to fill these gaps. A more complete understanding of MMP roles, particularly with regards to upstream signaling roles, may provide new strategies to limit adverse LV remodeling.
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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.