Evidence map›Paper›PMID 34640448›Full record

ReviewJournal of clinical medicine2021

A Review of the Molecular Mechanisms Underlying Cardiac Fibrosis and Atrial Fibrillation.

Grażyna Sygitowicz, Agata Maciejak-Jastrzębska, Dariusz Sitkiewicz

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
6.5field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 97 citations in OpenAlex.

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  11. A novel technique for vein of Marshall blood sampling and its application in assessing atrial remodeling in atrial fibrillation.Clinical research in cardiology : official journal of the German Cardiac Society · 2025
    Article
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  15. Journal of thoracic disease · 2025
    Article
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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

3 authors at 1 institution in 1 country.

Grażyna SygitowiczDepartment of Clinical Chemistry and Laboratory Diagnostics, Medical University of Warsaw, 02-097 Warsaw, Poland.ORCID 0000-0002-0057-4253
Agata Maciejak-JastrzębskaDepartment of Clinical Chemistry and Laboratory Diagnostics, Medical University of Warsaw, 02-097 Warsaw, Poland.
Dariusz SitkiewiczDepartment of Clinical Chemistry and Laboratory Diagnostics, Medical University of Warsaw, 02-097 Warsaw, Poland.
Medical University of Warsaw · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cellular and molecular mechanism involved in the pathogenesis of atrial fibrosis are highly complex. We have reviewed the literature that covers the effectors, signal transduction and physiopathogenesis concerning extracellular matrix (ECM) dysregulation and atrial fibrosis in atrial fibrillation (AF). At the molecular level: angiotensin II, transforming growth factor-β1, inflammation, and oxidative stress are particularly important for ECM dysregulation and atrial fibrotic remodelling in AF. We conclude that the Ang-II-MAPK and TGF-β1-Smad signalling pathways play a major, central role in regulating atrial fibrotic remodelling in AF. The above signalling pathways induce the expression of genes encoding profibrotic molecules (MMP, CTGF, TGF-β1). An important mechanism is also the generation of reactive oxygen species. This pathway induced by the interaction of Ang II with the AT

Indexed as

atrial fibrillationcardiac fibrosismiRNAsMMPsneurohormonal mechanisms

Identifiers

PMID34640448
PMCPMC8509789
OpenAlexW3203271056

What Socratic 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 Socratic graph.