Evidence map›Paper›PMID 36531712›Full record

ArticleFrontiers in cardiovascular medicine2022

Transcriptome and proteome profiling of activated cardiac fibroblasts supports target prioritization in cardiac fibrosis.

Maria Raquel Moita, Marta M Silva, Cláudia Diniz, Margarida Serra, René M Hoet, Ana Barbas, Daniel Simão

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Acute kidney injury disrupts cardiac remodeling via SerpinA3N.bioRxiv : the preprint server for biology · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Nanomedicine for Diagnosis and Treatment of Cardiac Fibrosis.International journal of nanomedicine · 2025
    Review
  9. Article
  10. Review
  11. Article
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

7 authors at 3 institutions in 2 countries.

Maria Raquel MoitaiBET - Instituto de Biologia Experimental e Tecnológica, Oeiras, Portugal.
Marta M SilvaiBET - Instituto de Biologia Experimental e Tecnológica, Oeiras, Portugal.
Cláudia DiniziBET - Instituto de Biologia Experimental e Tecnológica, Oeiras, Portugal.
Margarida SerraiBET - Instituto de Biologia Experimental e Tecnológica, Oeiras, Portugal.
René M HoetDepartment of Pathology, CARIM - School of Cardiovascular Diseases, Maastricht University, Maastricht, Netherlands.
Ana BarbasBayer Portugal, Carnaxide, Portugal.
Daniel SimãoiBET - Instituto de Biologia Experimental e Tecnológica, Oeiras, Portugal.
Instituto de Biologia Experimental e Tecnológica · PTUniversidade Nova de Lisboa · PTMaastricht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Activated cardiac fibroblasts (CF) play a central role in cardiac fibrosis, a condition associated with most cardiovascular diseases. Conversion of quiescent into activated CF sustains heart integrity upon injury. However, permanence of CF in active state inflicts deleterious heart function effects. Mechanisms underlying this cell state conversion are still not fully disclosed, contributing to a limited target space and lack of effective anti-fibrotic therapies. Materials and methods: To prioritize targets for drug development, we studied CF remodeling upon activation at transcriptomic and proteomic levels, using three different cell sources: primary adult CF (aHCF), primary fetal CF (fHCF), and induced pluripotent stem cells derived CF (hiPSC-CF). Results: All cell sources showed a convergent response upon activation, with clear morphological and molecular remodeling associated with cell-cell and cell-matrix interactions. Quantitative proteomic analysis identified known cardiac fibrosis markers, such as FN1, CCN2, and Serpine1, but also revealed targets not previously associated with this condition, including MRC2, IGFBP7, and NT5DC2. Conclusion: Exploring such targets to modulate CF phenotype represents a valuable opportunity for development of anti-fibrotic therapies. Also, we demonstrate that hiPSC-CF is a suitable cell source for preclinical research, displaying significantly lower basal activation level relative to primary cells, while being able to elicit a convergent response upon stimuli.

Indexed as

cardiac fibroblastcardiac fibrosismyofibroblastquantitative proteomicstranscriptomic

Identifiers

PMID36531712
PMCPMC9751336
OpenAlexW4311047831

What OpenQuestion holds

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LicenceCC BY
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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.