Evidence map›Paper›PMID 19134193›Full record

SynthesisBMC genomics2009

Reconstruction and functional analysis of altered molecular pathways in human atherosclerotic arteries.

Stefano Cagnin, Michele Biscuola, Cristina Patuzzo, Elisabetta Trabetti, Alessandra Pasquali, Paolo Laveder, Giuseppe Faggian, Mauro Iafrancesco, Alessandro Mazzucco, Pier Franco Pignatti and 1 more

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in BMC genomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 94 citations in OpenAlex.

  1. Review
  2. Macrophage HM13/SPP Enhances Foamy Macrophage Formation and Atherogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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  18. A Network Pharmacology Technique to Investigate the Synergistic Mechanisms ofEvidence-based complementary and alternative medicine : eCAM · 2020
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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

11 authors at 2 institutions in 1 country.

Stefano CagninCRIBI Biotechnology Centre, University of Padova, Padova, Italy. stefanoc@cribi.unipd.it
Michele Biscuola
Cristina Patuzzo
Elisabetta Trabetti
Alessandra Pasquali
Paolo Laveder
Giuseppe Faggian
Mauro Iafrancesco
Alessandro Mazzucco
Pier Franco Pignatti
Gerolamo Lanfranchi
University of Verona · ITUniversity of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAtherosclerosis affects aorta, coronary, carotid, and iliac arteries most frequently than any other body vessel. There may be common molecular pathways sustaining this process. Plaque presence and diffusion is revealed by circulating factors that can mediate systemic reaction leading to plaque rupture and thrombosis.

resultsWe used DNA microarrays and meta-analysis to study how the presence of calcified plaque modifies human coronary and carotid gene expression. We identified a series of potential human atherogenic genes that are integrated in functional networks involved in atherosclerosis. Caveolae and JAK/STAT pathways, and S100A9/S100A8 interacting proteins are certainly involved in the development of vascular disease. We found that the system of caveolae is directly connected with genes that respond to hormone receptors, and indirectly with the apoptosis pathway. Cytokines, chemokines and growth factors released in the blood flux were investigated in parallel. High levels of RANTES, IL-1ra, MIP-1 alpha, MIP-1 beta, IL-2, IL-4, IL-5, IL-6, IL-7, IL-17, PDGF-BB, VEGF and IFN-gamma were found in plasma of atherosclerotic patients and might also be integrated in the molecular networks underlying atherosclerotic modifications of these vessels.

conclusionThe pattern of cytokine and S100A9/S100A8 up-regulation characterizes atherosclerosis as a proinflammatory disorder. Activation of the JAK/STAT pathway is confirmed by the up-regulation of IL-6, STAT1, ISGF3G and IL10RA genes in coronary and carotid plaques. The functional network constructed in our research is an evidence of the central role of STAT protein and the caveolae system to contribute to preserve the plaque. Moreover, Cav-1 is involved in SMC differentiation and dyslipidemia confirming the importance of lipid homeostasis in the atherosclerotic phenotype.

Indexed as

AdultAgedAtherosclerosisCalgranulin ACalgranulin BCarotid ArteriesCaveolaeCoronary VesselsCytokinesFemaleGene ExpressionGene Expression ProfilingHumansMaleMiddle AgedOligonucleotide Array Sequence AnalysisCalgranulin ACalgranulin BCytokinesSTAT Transcription Factors

Identifiers

PMID19134193
PMCPMC2654039
OpenAlexW1983390546

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.