Evidence map›Paper›PMID 41290770›Full record

ArticleScientific reports2025

Profiling of main regulators of angiogenesis and inflammation in human PBMC and plasma revealed associations with lower extremity artery disease.

Daniel Zalewski, Paulina Chmiel, Przemysław Kołodziej, Marcin Feldo, Jacek Bogucki, Janusz Kocki, Anna Bogucka-Kocka

Abstract read
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In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Daniel ZalewskiChair and Department of Biology and Genetics, Medical University of Lublin, 4a Chodźki St., Lublin, 20-093, Poland. daniel.zalewski@umlub.pl.
Paulina ChmielChair and Department of Biology and Genetics, Medical University of Lublin, 4a Chodźki St., Lublin, 20-093, Poland.
Przemysław KołodziejLaboratory of Diagnostic Parasitology, Chair and Department of Biology and Genetics, Medical University of Lublin, 4a Chodźki St., Lublin, 20-093, Poland.
Marcin FeldoChair and Department of Vascular Surgery and Angiology, Medical University of Lublin, 8 Solidarności St., Lublin, 20-841, Poland.
Jacek BoguckiInstitute of Medical Sciences, The John Paul II (The Second) Catholic University of Lublin, Konstantynów 1F St., Lublin, 20-708, Poland.
Janusz KockiDepartment of Clinical Genetics, Chair of Medical Genetics, Medical University of Lublin, 11 Radziwiłłowska St., Lublin, 20-080, Poland.
Anna Bogucka-KockaChair and Department of Biology and Genetics, Medical University of Lublin, 4a Chodźki St., Lublin, 20-093, Poland.

Funding

Uniwersytet Medyczny w Lublinie DS43Uniwersytet Medyczny w Lublinie PBsd40 (registration number GW/PB/13/2021)
6 · The paper itself

Abstract

Lower extremity artery disease (LEAD) represents the most common atherosclerosis-related disease in the group of peripheral artery diseases. A growing amount of evidence suggests that dysregulations in signaling pathways associated with angiogenesis and inflammation can contribute to the progression and onset of LEAD; however, this association is still poorly understood. Therefore, in our study, we investigated expression levels of 18 genes that encode key regulators of angiogenesis and inflammation, as well as plasma levels of their protein products, in patients with LEAD in comparison with non-LEAD controls. Gene expression levels were determined in peripheral blood mononuclear cells (PBMC) using real-time PCR, and protein plasma levels were measured using ELISA. The expression levels of TGFB1, VEGFA, and VEGFB, as well as the plasma concentrations of ANG-1, CCL2, PDGF-AB, TGF-beta 1, and TNF-alpha, significantly differentiated the LEAD group from the control group. A strong correlation was found between the expression levels of TGFB1 and VEGFA. Significant relationships between VEGFB expression and blood cholesterol levels, as well as between CCL2 plasma concentrations and C-reactive protein blood levels, were demonstrated. Identified dysregulations in key angiogenesis and inflammation-related factors could reflect abnormal regulation of these processes in patients with LEAD, shedding new light on the molecular mechanisms underlying the development of LEAD and indicating candidates for circulatory biomarkers of this disease.

Indexed as

InflammationLeukocytes, MononuclearLower ExtremityNeovascularization, PathologicPeripheral Arterial DiseaseAgedAngiogenesisBiomarkersCase-Control StudiesFemaleHumansMaleMiddle AgedTransforming Growth Factor beta1Vascular Endothelial Growth Factor ABiomarkersTransforming Growth Factor beta1Vascular Endothelial Growth Factor AAngiogenesisGene expressionInflammationLower extremity artery diseasePeripheral artery diseasePlasma proteins

Identifiers

PMID41290770
PMCPMC12647588

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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.