Evidence map›Paper›PMID 38205347›Full record

ArticleJACC. Basic to translational science2023

Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction.

Sean A Hardy, Laura Liesinger, Ralph Patrick, Maria Poettler, Lavinia Rech, Juergen Gindlhuber, Nishani S Mabotuwana, DiyaaEldin Ashour, Verena Stangl, Mark Bigland and 11 more

Open access · goldAbstract read
In one paragraph

Article in JACC. Basic to translational science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.6field-weighted citation impact, top 4% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Retinol saturase in the mitochondria antagonizes IDH2 and GLUD1 acetylation to mediate heart repair.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. RNA 5-Methylcytosine Modification in Myocardial Fibrosis.Reviews in cardiovascular medicine · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Frontiers in cardiovascular medicine · 2025
    Article
  11. Article
  12. Review
  13. Article
  14. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

21 authors at 10 institutions in 4 countries.

Sean A HardyDepartment of Internal Medicine and University Heart Center, Division of Cardiology, Medical University of Graz, Graz, Austria.
Laura LiesingerDiagnostic and Research Institute of Pathology, Medical University of Graz, Graz, Austria.
Ralph PatrickSchool of Clinical Medicine, Faculty of Medicine and Health, University of New South Wales, Sydney, New South Wales, Australia.
Maria PoettlerDepartment of Internal Medicine and University Heart Center, Division of Cardiology, Medical University of Graz, Graz, Austria.
Lavinia RechDepartment of Internal Medicine and University Heart Center, Division of Cardiology, Medical University of Graz, Graz, Austria.
Juergen GindlhuberLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.
Nishani S MabotuwanaDepartment of Internal Medicine and University Heart Center, Division of Cardiology, Medical University of Graz, Graz, Austria.
DiyaaEldin AshourComprehensive Heart Failure Center, University Hospital Würzburg, Würzburg, Germany.
Verena StanglDiagnostic and Research Institute of Pathology, Medical University of Graz, Graz, Austria.
Mark BiglandSchool of Medicine and Public Health, University of Newcastle, Callaghan, New South Wales, Australia.
Lucy A MurthaSchool of Medicine and Public Health, University of Newcastle, Callaghan, New South Wales, Australia.
Malcolm R StarkeyDepartment of Immunology, Central Clinical School, Monash University, Melbourne, Victoria, Australia.
Daniel ScherrDepartment of Internal Medicine and University Heart Center, Division of Cardiology, Medical University of Graz, Graz, Austria.
Philip M HansbroCentre for Inflammation, Centenary Institute, and University of Technology Sydney, Faculty of Science, School of Life Sciences, Sydney, New South Wales, Australia.
Gerald HoeflerDiagnostic and Research Institute of Pathology, Medical University of Graz, Graz, Austria.
Gustavo Campos RamosComprehensive Heart Failure Center, University Hospital Würzburg, Würzburg, Germany.
Clement CochainComprehensive Heart Failure Center, University Hospital Würzburg, Würzburg, Germany.
Richard P HarveySchool of Clinical Medicine, Faculty of Medicine and Health, University of New South Wales, Sydney, New South Wales, Australia.
Ruth Birner-GruenbergerDiagnostic and Research Institute of Pathology, Medical University of Graz, Graz, Austria.
Andrew J BoyleSchool of Medicine and Public Health, University of Newcastle, Callaghan, New South Wales, Australia.
Peter P RainerDepartment of Internal Medicine and University Heart Center, Division of Cardiology, Medical University of Graz, Graz, Austria.
Medical University of Graz · ATUniversitätsklinikum Würzburg · DEHunter Medical Research Institute · AUTU Wien · ATUNSW Sydney · AUBoston Children's Hospital · USJohn Hunter Hospital · AULudwig Boltzmann Institute for Lung Vascular Research · ATMonash University · AUUniversity of Technology Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Irreversible fibrosis is a hallmark of myocardial infarction (MI) and heart failure. Extracellular matrix protein-1 (ECM-1) is up-regulated in these hearts, localized to fibrotic, inflammatory, and perivascular areas. ECM-1 originates predominantly from fibroblasts, macrophages, and pericytes/vascular cells in uninjured human and mouse hearts, and from M1 and M2 macrophages and myofibroblasts after MI. ECM-1 stimulates fibroblast-to-myofibroblast transition, up-regulates key fibrotic and inflammatory pathways, and inhibits cardiac fibroblast migration. ECM-1 binds HuCFb cell surface receptor LRP1, and LRP1 inhibition blocks ECM-1 from stimulating fibroblast-to-myofibroblast transition, confirming a novel ECM-1-LRP1 fibrotic signaling axis. ECM-1 may represent a novel mechanism facilitating inflammation-fibrosis crosstalk.

Indexed as

extracellular matrixfibroblastsfibrosisheartinflammationmyocardial infarction

Identifiers

PMID38205347
PMCPMC10774582
OpenAlexW4385858468

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.