ArticleeLife2020
Macrophages promote endothelial-to-mesenchymal transition via MT1-MMP/TGFβ1 after myocardial infarction.
Open access · goldAbstract read
In one paragraph
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
6.1field-weighted citation impact, top 2% of its field
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
64 citing papers in PubMed, 82 citations in OpenAlex.
- SGLT2 inhibitors: mechanisms, physiology and pharmacology, and clinical applications.Molecular biomedicine · 2026Review
- The inflammatory/fibrotic axis across organs: myelofibrosis as a model of reversibility.JCI insight · 2026Review
- M2 Macrophage Polarization Characterizes an Immunosuppressive Microenvironment in Extracranial Arteriovenous Malformations.Biomedicines · 2026Article
- Human stem cell models in cerebral cavernous malformations.Stem cell research & therapy · 2026Review
- A miR-200b-Filamin A axis drives epicardial contribution to cardiogenesis.Scientific reports · 2026Article
- EndMT in vascular cognitive impairment and dementia: mechanisms, evidence gaps, and therapeutic opportunities.Molecular medicine (Cambridge, Mass.) · 2026Review
- Oscillatory shear stress-driven endothelial-to-mesenchymal transition: a critical mechanical signal transduction mechanism in atherosclerosis progression.Cell death discovery · 2026Review
- M2 macrophages promote heterotopic ossification through MSX2 binding to LEF1-mediated endothelial-mesenchymal transition.Stem cell research & therapy · 2026Article
- Obesity-Associated Cardiac Fibrosis: Mechanisms and Emerging Therapeutic Targets.Vascular health and risk management · 2026Review
- Hypoxia-driven crosstalk among cardiac fibroblasts, macrophages, and endothelial cells in cardiac fibrosis.Frontiers in cell and developmental biology · 2026Review
- MMP14-Dependent Activation of TGF-β Signaling Enhances Malignancies via Promoting Necroptosis in Glioblastoma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Exercise-induced hypertrophic preconditioning alleviates myocardial ischemic injury through trained immunity of macrophages.Journal of translational medicine · 2025Article
- Review
- Biofabrication of a 3D human skeletal muscle microenvironment to study the early steps of fibrosis.Materials today. Bio · 2025Article
- Heterogeneity and characteristic changes in cardiomyocytes and non‑cardiomyocytes following myocardial infarction: Insights from single‑cell sequencing analysis (Review).Molecular medicine reports · 2025Review
- Macrophage ITGAV is dispensable for post-infarction remodeling in mice and does not mediate fibronectin responses.Communications biology · 2025Article
- Baricitinib and Infliximab Mitigate the Endothelial-to-Mesenchymal Transition (EndMT) Induced by Cytokines in HUVECs.International journal of molecular sciences · 2025Article
- Cardiac Macrophages Promote Polarization of Macrophages toward M2 Phenotype to Improve Myocardial Remodeling via NGAL after Myocardial Infarction.Cell biochemistry and biophysics · 2025Article
- The Immune Microenvironment: New Therapeutic Implications in Organ Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Post-myocardial Infarction Cardiac Remodeling: Multidimensional Mechanisms and Clinical Prospects of Stem Cell Therapy.Stem cell reviews and reports · 2025Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
13 authors at 2 institutions in 1 country.
Laura Alonso-HerranzMyocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.ORCID 0000-0003-0880-4735
Álvaro Sahún-EspañolVascular Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.ORCID 0000-0003-3833-5386
Ana ParedesMyocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.ORCID 0000-0003-3119-8788
Pilar GonzaloVascular Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.ORCID 0000-0001-8811-8369
Polyxeni GkontraVascular Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Vanessa NúñezMyocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Cristina ClementeVascular Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.ORCID 0000-0002-5831-9132
Marta CedenillaMyocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
María Villalba-OreroMyocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Javier InserteCardiovascular Diseases Research Group, Vall d'Hebron University Hospital and Research Institute (VHIR), Barcelona, Spain.
David García-DoradoCardiovascular Diseases Research Group, Vall d'Hebron University Hospital and Research Institute (VHIR), Barcelona, Spain.
Alicia G ArroyoVascular Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.ORCID 0000-0002-1536-3846
Mercedes RicoteMyocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.ORCID 0000-0002-8090-8902
Spanish National Centre for Cardiovascular Research · ESCentro de Investigación en Red en Enfermedades Cardiovasculares · ES
Funding
Comunidad de Madrid MOIR-B2017/BMD-3684Spanish Ministry of Science and Innovation BES-2016-076632Spanish Ministry of Science, Innovation and Universities RTI2018-095928-BI00Spanish Ministry of Science, Innovation and Universities SAF2017-83229-RSpanish Ministry of Science, Innovation and Universities SAF2017-90604-REDT-NurCaMeinSpanish Ministry of Science, Innovation and Universities SAF2017-90604-REDT-NurCaMeIn
Abstract
Macrophages (Mφs) produce factors that participate in cardiac repair and remodeling after myocardial infarction (MI); however, how these factors crosstalk with other cell types mediating repair is not fully understood. Here we demonstrated that cardiac Mφs increased the expression of
Indexed as
Epithelial-Mesenchymal TransitionAnimalsCollagenDisease Models, AnimalEndothelium, VascularFemaleFibrosisFlow CytometryGene Expression RegulationHEK293 CellsHumansMacrophagesMaleMatrix Metalloproteinase 14MiceMice, Inbred C57BLCollagenMatrix Metalloproteinase 14Mmp14 protein, mouseTgfb1 protein, mouseTransforming Growth Factor beta1endothelial cellsimmunologyinflammationmacrophagesmouseMT1-MMPmyocardial infarctionregenerative medicinestem cellsTGFB1tissue remodeling
Identifiers
What OpenQuestion holds
Textmetadata
LicenceCC BY
Read underepoch 390
Registered trials
None linked
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.