Evidence map›Paper›PMID 23448358›Full record

ArticleFibrogenesis & tissue repair2013

Function and fate of myofibroblasts after myocardial infarction.

Neil A Turner, Karen E Porter

Open access · hybridAbstract read
In one paragraph

Article in Fibrogenesis & tissue repair, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
10.5field-weighted citation impact, top 1% 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

88 citing papers in PubMed, 173 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Molecular contrast agents for post-infarct cardiac remodelling: a contemporary review.European heart journal. Imaging methods and practice · 2026
    Review
  5. Article
  6. Review
  7. Review
  8. Expression ofGenes · 2024
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Intramyocardial immunomodulation with human CD16Frontiers in cardiovascular medicine · 2024
    Article
  14. Article
  15. Review
  16. p53 and Myofibroblast Apoptosis in Organ Fibrosis.International journal of molecular sciences · 2023
    Review
  17. Activating α7nAChR helps post-myocardial infarction healing by regulating macrophage polarization via the STAT3 signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  18. Article
  19. Article
  20. Article

28 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Neil A TurnerDivision of Cardiovascular and Diabetes Research, and Multidisciplinary Cardiovascular Research Centre, School of Medicine, University of Leeds, Leeds LS2 9JT, UK. n.a.turner@leeds.ac.uk.
Karen E Porter
University of Leeds · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The importance of cardiac fibroblasts in the regulation of myocardial remodelling following myocardial infarction (MI) is becoming increasingly recognised. Studies over the last few decades have reinforced the concept that cardiac fibroblasts are much more than simple homeostatic regulators of extracellular matrix turnover, but are integrally involved in all aspects of the repair and remodelling of the heart that occurs following MI. The plasticity of fibroblasts is due in part to their ability to undergo differentiation into myofibroblasts. Myofibroblasts are specialised cells that possess a more contractile and synthetic phenotype than fibroblasts, enabling them to effectively repair and remodel the cardiac interstitium to manage the local devastation caused by MI. However, in addition to their key role in cardiac restoration and healing, persistence of myofibroblast activation can drive pathological fibrosis, resulting in arrhythmias, myocardial stiffness and progression to heart failure. The aim of this review is to give an appreciation of both the beneficial and detrimental roles of the myofibroblast in the remodelling heart, to describe some of the major regulatory mechanisms controlling myofibroblast differentiation including recent advances in the microRNA field, and to consider how this cell type could be exploited therapeutically.

Identifiers

PMID23448358
PMCPMC3599637
OpenAlexW2134265214

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.