Evidence map›Paper›PMID 27144566›Full record

ArticleInternational journal of molecular sciences2016

Label-Free Quantitative Proteomics Reveals Differences in Molecular Mechanism of Atherosclerosis Related and Non-Related to Chronic Kidney Disease.

Magdalena Luczak, Joanna Suszynska-Zajczyk, Lukasz Marczak, Dorota Formanowicz, Elzbieta Pawliczak, Maria Wanic-Kossowska, Maciej Stobiecki

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

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  12. Osteopontin: The Molecular Bridge between Fat and Cardiac-Renal Disorders.International journal of molecular sciences · 2020
    Review
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  18. Advances in Chronic Kidney Disease.International journal of molecular sciences · 2016
    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

7 authors at 3 institutions in 1 country.

Magdalena LuczakEuropean Centre for Bioinformatics and Genomics, Institute of Bioorganic Chemistry, Polish Academy of Sciences, Noskowskiego 12/14, 61-704 Poznan, Poland. magdalena.luczak@put.poznan.pl.
Joanna Suszynska-ZajczykDepartment of Biochemistry and Biotechnology, Poznan University of Life Sciences, Dojazd 11, 60-632 Poznan, Poland. suszynska@yahoo.co.uk.
Lukasz MarczakEuropean Centre for Bioinformatics and Genomics, Institute of Bioorganic Chemistry, Polish Academy of Sciences, Noskowskiego 12/14, 61-704 Poznan, Poland. lukasmar@ibch.poznan.pl.
Dorota FormanowiczDepartment of Clinical Biochemistry and Laboratory Medicine, Poznan University of Medical Sciences, Grunwaldzka 6, 60-780 Poznan, Poland. doforman@ump.edu.pl.
Elzbieta PawliczakDepartment of Nephrology, Transplantology and Internal Medicine, Poznan University of Medical Sciences, Przybyszewskiego 49, 60-355 Poznan, Poland. epawliczak@wp.pl.
Maria Wanic-KossowskaDepartment of Nephrology, Transplantology and Internal Medicine, Poznan University of Medical Sciences, Przybyszewskiego 49, 60-355 Poznan, Poland. wanic.kossowska.maria@gmail.com.
Maciej StobieckiEuropean Centre for Bioinformatics and Genomics, Institute of Bioorganic Chemistry, Polish Academy of Sciences, Noskowskiego 12/14, 61-704 Poznan, Poland. mackis@ibch.poznan.pl.
Institute of Bioorganic Chemistry, Polish Academy of Sciences · PLPoznan University of Medical Sciences · PLUniversity of Life Sciences in Poznań · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The major cause of mortality in patients with chronic kidney disease (CKD) is atherosclerosis related to traditional and non-traditional risk factors. However, the understanding of the molecular specificity that distinguishes the risk factors for classical cardiovascular disease (CVD) and CKD-related atherosclerosis (CKD-A) is far from complete. In this study we investigated the disease-related differences in the proteomes of patients with atherosclerosis related and non-related to CKD. Plasma collected from patients in various stages of CKD, CVD patients without symptoms of kidney dysfunction, and healthy volunteers (HVs), were analyzed by a coupled label-free and mass spectrometry approach. Dysregulated proteins were confirmed by an enzyme-linked immunosorbent assay (ELISA). All proteomic data were correlated with kidney disease development and were subjected to bioinformatics analysis. One hundred sixty-two differentially expressed proteins were identified. By directly comparing the plasma proteomes from HVs, CKD, and CVD patients in one study, we demonstrated that proteins involved in inflammation, blood coagulation, oxidative stress, vascular damage, and calcification process exhibited greater alterations in patients with atherosclerosis related with CKD. These data indicate that the above nontraditional risk factors are strongly specific for CKD-A and appear to be less essential for the development of "classical" CVD.

Indexed as

Proteomicsalpha-2-HS-GlycoproteinAtherosclerosisCase-Control StudiesChromatography, High Pressure LiquidEnzyme-Linked Immunosorbent AssayHumansOsteopontinPeroxiredoxinsPrincipal Component AnalysisRenal Insufficiency, ChronicRisk FactorsTandem Mass Spectrometryalpha-2-HS-GlycoproteinOsteopontinPeroxiredoxinsatherosclerosiscardiovascular diseasechronic kidney diseaselabel-free quantitative proteomics

Identifiers

PMID27144566
PMCPMC4881457
OpenAlexW2346120897

What OpenQuestion holds

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LicenceCC BY
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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.