Evidence map›Paper›PMID 18194448›Full record

ArticleJournal of cellular and molecular medicine

Atrial extracellular matrix remodelling in patients with atrial fibrillation.

V Polyakova, S Miyagawa, Z Szalay, J Risteli, S Kostin

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

69 citing papers in PubMed, 143 citations in OpenAlex.

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  6. Beyond CHAAnnals of biomedical engineering · 2026
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  14. Cardiac Arrhythmia: Molecular Mechanisms and Therapeutic Strategies.International journal of molecular sciences · 2024
    Article
  15. Atrial fibrillation in human patients is associated with increased collagen type V and TGFbeta1.International journal of cardiology. Heart & vasculature · 2024
    Article
  16. Article
  17. Article
  18. Review
  19. Atrial Fibrillation: Rate Versus Rhythm Control.HCA healthcare journal of medicine · 2023
    Review
  20. Article

9 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

5 authors at 3 institutions in 3 countries.

V PolyakovaMax-Planck-Institute for Heart and Lung Research, Core Lab for Molecular and Structural Biology, Bad Nauheim, Germany.
S Miyagawa
Z Szalay
J Risteli
S Kostin
Kerckhoff Klinik · DEMax Planck Institute for Heart and Lung Research · DEUniversity of Oulu · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledAtrial fibrillation (AF) is the most frequent clinical arrhythmia. Atrial fibrosis is an important factor in initiating and maintaining AF. However, the collagen turnover and its regulation in AF has not been completely elucidated. We tested the hypothesis that the extracellular matrix changes are more severe in patients with permanent AF in comparison with those in patients in sinus rhythm (SR). Intraoperative biopsies from the right atrial appendages (RAA) and free walls (RFW) from 24 patients with AF undergoing a mini-Maze procedure and 24 patients in SR were investigated with qualitative and quantitative immunofluorescent and Western blot analyses. As compared with SR, all patients with AF exhibited dysregulations in collagen type I and type III synthesis/degradation. Tissue inhibitors of metalloproteinases (TIMP2) was significantly enhanced only in RAA-AF. As compared with SR, collagen VI, matrix metalloproteinases MMP2, MMP9 and TIMP1 were significantly increased while TIMP3 and TIMP4 remained unchanged in all AF groups. Reversion-inducing cysteine-rich protein with Kazal motifs (RECK), a newly discovered MMPs inhibitor, was elevated in RFW as compared to RAA-AF (P<0.05) and RFW-SR (P<0.05). The level of transforming growth factor (TGF)-beta1 was higher in AF than SR. Smad2 and phosphorylated Smad2 showed an elevation in RFW-AF as compared to RFW-SR, RAA-AF, and RAA-SR groups (P<0.05).

conclusionsAtrial fibrosis in AF is characterized by severe alterations in collagen I and III synthesis/degradation associated with disturbed MMP/TIMP systems and increased levels of RECK. TGF-beta1 contributes to atrial fibrosis via TGF-beta1-Smad pathway by phosphorylating Smad2. These processes culminate in accumulations of fibrillar and non-fibrillar collagens leading to excessive atrial fibrosis and maintainance of AF.

Indexed as

AgedAtrial AppendageAtrial FibrillationBlotting, WesternCollagen Type IExtracellular MatrixFemaleFluorescent Antibody TechniqueGPI-Linked ProteinsHumansMaleMatrix Metalloproteinase 2Matrix Metalloproteinase 9Membrane GlycoproteinsMiddle AgedPhosphorylationCollagen Type IGPI-Linked ProteinsMatrix Metalloproteinase 2Matrix Metalloproteinase 9Membrane GlycoproteinsRECK protein, humanSmad2 ProteinSMAD2 protein, humanTissue Inhibitor of Metalloproteinase-2Transforming Growth Factor beta1

Identifiers

PMID18194448
PMCPMC3823481
OpenAlexW2170459650

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.