Evidence map›Paper›PMID 42120549›Full record

ArticleScientific reports2026

Loss of IGFBP-6 promotes monocyte-driven atherogenesis in periodontal disease.

Dáire Shanahan, Georgios Kremastiotis, Kerry Wadey, Claudine Hodgson, Joon Seong, Nicola West, Angela H Nobbs, Jason Johnson, Sarah George

Abstract read
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In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

9 authors.

Dáire ShanahanLaboratory of Cardiovascular Pathology, Translational Health Sciences, Bristol Medical School, University of Bristol, Level 7 Bristol Royal Infirmary, Bristol, UK. daire.shanahan@bristol.ac.uk.
Georgios KremastiotisLaboratory of Cardiovascular Pathology, Translational Health Sciences, Bristol Medical School, University of Bristol, Level 7 Bristol Royal Infirmary, Bristol, UK.
Kerry WadeyLaboratory of Cardiovascular Pathology, Translational Health Sciences, Bristol Medical School, University of Bristol, Level 7 Bristol Royal Infirmary, Bristol, UK.
Claudine HodgsonLaboratory of Cardiovascular Pathology, Translational Health Sciences, Bristol Medical School, University of Bristol, Level 7 Bristol Royal Infirmary, Bristol, UK.
Joon SeongBristol Dental School, University of Bristol, 1 Trinity Quay, Avon Street, Bristol, BS2 0PT, UK.
Nicola WestBristol Dental School, University of Bristol, 1 Trinity Quay, Avon Street, Bristol, BS2 0PT, UK.
Angela H NobbsBristol Dental School Research Laboratories, Dorothy Hodgkin Building, University of Bristol, Bristol, BS1 3NY, UK.
Jason JohnsonLaboratory of Cardiovascular Pathology, Translational Health Sciences, Bristol Medical School, University of Bristol, Level 7 Bristol Royal Infirmary, Bristol, UK.
Sarah GeorgeLaboratory of Cardiovascular Pathology, Translational Health Sciences, Bristol Medical School, University of Bristol, Level 7 Bristol Royal Infirmary, Bristol, UK.

Funding

Medical Research Council MR/V002007/1
6 · The paper itself

Abstract

Periodontitis has been associated with an increased risk of atherosclerosis, potentially through altered systemic monocyte and macrophage function. We aimed to identify a differentially expressed protein in naïve monocytes from individuals with periodontitis compared to controls and investigate its association with pro-atherosclerotic monocyte and macrophage functions. Peripheral blood monocytes were isolated from individuals with periodontitis and matched controls. Proteomic analysis and bioinformatics identified insulin-like growth factor-binding protein-6 (IGFBP-6) as a protein of interest. IGFBP-6 protein was quantified in monocytes, macrophages, foam cells, and plasma using Western blotting. To model periodontitis in vitro, monocytes and macrophages were treated with Porphyromonas gingivalis lipopolysaccharide. Extracellular vesicles were analysed for IGFBP-6 content and activity. Foam cell formation, cholesterol transporter expression, monocyte adhesion, macrophage transmigration, inflammatory cytokine production, and apoptosis were quantified. IGFBP-6 levels were reduced intracellularly but elevated in plasma in periodontitis, and similar patterns were observed in lipopolysaccharide-treated cells. IGFBP-6 in extracellular vesicles lacked biological activity. Reduced IGFBP-6 protein was associated with increased foam cell formation and downregulation of ATP-binding cassette subfamily-G1 (ABCG1), independent of IGF signalling. Restoration of IGFBP-6 was associated with reduced foam cell formation and inflammation, alongside inhibition of macrophage transmigration. These findings suggest that altered IGFBP-6 levels may contribute to the progression of atherosclerosis in periodontitis.

Indexed as

AtherosclerosisInsulin-Like Growth Factor Binding Protein 6MonocytesPeriodontal DiseasesPeriodontitisATP Binding Cassette Transporter, Subfamily G, Member 1FemaleFoam CellsHumansLipopolysaccharidesMacrophagesMaleMiddle AgedPorphyromonas gingivalisABCG1 protein, humanATP Binding Cassette Transporter, Subfamily G, Member 1Insulin-Like Growth Factor Binding Protein 6LipopolysaccharidesABCG12Atherosclerosis3IGFBP-61Macrophage6Monocyte5Periodontitis4

Identifiers

PMID42120549
PMCPMC13357806

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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.