Evidence map›Paper›PMID 24321195›Full record

ReviewJournal of molecular and cellular cardiology2014

Fibroblasts in myocardial infarction: a role in inflammation and repair.

Arti V Shinde, Nikolaos G Frangogiannis

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 303 papers.

0numbers the graph read from it
0cells of the map it votes in
303citing papers in PubMed
17.6field-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

303 citing papers in PubMed, 506 citations in OpenAlex.

  1. Article
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  5. [A new method for extracting adult mouse cardiac fibroblasts more efficiently and stably].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2026
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  14. NF-Frontiers in cardiovascular medicine · 2026
    Review
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243 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.

Arti V ShindeThe Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), Albert Einstein College of Medicine, Bronx, NY, USA.
Nikolaos G FrangogiannisThe Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), Albert Einstein College of Medicine, Bronx, NY, USA. Electronic address: nikolaos.frangogiannis@einstein.yu.edu.
Albert Einstein College of Medicine · US

Funding

Chemokines in Healing Myocardial InfarctsR01HL076246 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI Nikolaos G Frangogiannis · 2005 to 2026
$9.5M
Resolution of Inflammation in healing Myocardial InfarctsR01HL085440 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI FRANGOGIANNIS, NIKOLAOS G · 2008 to 2025
$8.5M
NHLBI NIH HHS HL76246NHLBI NIH HHS R01 HL076246NHLBI NIH HHS R01 HL085440NHLBI NIH HHS R01 HL85440
6 · The paper itself

Abstract

Fibroblasts do not only serve as matrix-producing reparative cells, but exhibit a wide range of functions in inflammatory and immune responses, angiogenesis and neoplasia. The adult mammalian myocardium contains abundant fibroblasts enmeshed within the interstitial and perivascular extracellular matrix. The current review manuscript discusses the dynamic phenotypic and functional alterations of cardiac fibroblasts following myocardial infarction. Extensive necrosis of cardiomyocytes in the infarcted heart triggers an intense inflammatory reaction. In the early stages of infarct healing, fibroblasts become pro-inflammatory cells, activating the inflammasome and producing cytokines, chemokines and proteases. Pro-inflammatory cytokines (such as Interleukin-1) delay myofibroblast transformation, until the wound is cleared from dead cells and matrix debris. Resolution of the inflammatory infiltrate is associated with fibroblast migration, proliferation, matrix protein synthesis and myofibroblast conversion. Growth factors and matricellular proteins play an important role in myofibroblast activation during the proliferative phase of healing. Formation of a mature cross-linked scar is associated with clearance of fibroblasts, as poorly-understood inhibitory signals restrain the fibrotic response. However, in the non-infarcted remodeling myocardium, local fibroblasts may remain activated in response to volume and pressure overload and may promote interstitial fibrosis. Considering their abundance, their crucial role in cardiac inflammation and repair, and their involvement in myocardial dysfunction and arrhythmogenesis, cardiac fibroblasts may be key therapeutic targets in cardiac remodeling. This article is part of a Special Issue entitled Myocyte-Fibroblast Signalling in Myocardium.

Indexed as

Signal TransductionAnimalsCell MovementCell ProliferationCytokinesExtracellular MatrixExtracellular Matrix ProteinsFibroblastsGene Expression RegulationHumansInflammationIntercellular Signaling Peptides and ProteinsMyocardial InfarctionMyocardiumWound HealingCytokinesExtracellular Matrix ProteinsIntercellular Signaling Peptides and ProteinsCardiac remodelingExtracellular matrixFibroblastInflammationMyocardial infarctionTransforming growth factor (TGF)-β

Identifiers

PMID24321195
PMCPMC3995820
OpenAlexW2051521659

What OpenQuestion holds

Textmetadata
LicenceTDM
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.