Evidence map›Paper›PMID 33714552›Full record

ArticleAtherosclerosis2021

DNA glycosylase Neil3 regulates vascular smooth muscle cell biology during atherosclerosis development.

Ana Quiles-Jiménez, Ida Gregersen, Filip M Segers, Tonje Skarpengland, Penelope Kroustallaki, Kuan Yang, Xiang Yi Kong, Knut H Lauritzen, Maria B Olsen, Tom Rune Karlsen and 20 more

Open access · hybridAbstract read
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In one paragraph

Article in Atherosclerosis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Omics research in atherosclerosis.Molecular and cellular biochemistry · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

30 authors at 6 institutions in 3 countries.

Ana Quiles-JiménezResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway.
Ida GregersenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway.
Filip M SegersResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Department of Pharmacology, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Tonje SkarpenglandResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Penelope KroustallakiDepartment of Clinical Molecular Biology, University of Oslo, Akershus University Hospital, Lørenskog, Norway.
Kuan YangResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway.
Xiang Yi KongResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway.
Knut H LauritzenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Maria B OlsenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Tom Rune KarlsenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway.
Tuula A NymanDepartment of Immunology, Institute of Clinical Medicine, University of Oslo, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Ellen L SagenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Vigdis BjerkeliResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Rajikala SuganthanDepartment of Microbiology, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Ståle NygårdBioinformatics Core Facility, Institute for Medical Informatics, Oslo University Hospital, Oslo, Norway.
Katja SchefflerDepartment of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Jurriën PrinsEinthoven Laboratory of Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands; Department of Internal Medicine, Nephrology, Leiden University Medical Center, Leiden, the Netherlands.
Eric Van der VeerEinthoven Laboratory of Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands; Department of Internal Medicine, Nephrology, Leiden University Medical Center, Leiden, the Netherlands.
Jonas Ds ØgaardResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Yngvar FløisandDepartment of Hematology, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Helle F JørgensenDivision of Cardiovascular Medicine, Department of Medicine, University of Cambridge, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, Cambridge, United Kingdom.
Kirsten B HolvenNorwegian National Advisory Unit on Familial Hypercholesterolemia, Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Oslo, Norway; Faculty of Medicine, Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Erik A BiessenDepartment of Pathology, University of Maastricht, Maastricht, the Netherlands.
Hilde NilsenDepartment of Clinical Molecular Biology, University of Oslo, Akershus University Hospital, Lørenskog, Norway.
Tuva B DahlResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Sverre HolmResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Martin R BennettDivision of Cardiovascular Medicine, Department of Medicine, University of Cambridge, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, Cambridge, United Kingdom.
Pål AukrustResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway; Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Magnar BjøråsDepartment of Microbiology, Oslo University Hospital Rikshospitalet, Oslo, Norway; Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Bente HalvorsenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway. Electronic address: Bente.Halvorsen@rr-research.no.
Oslo University Hospital · NOLeiden University Medical Center · NLUniversity of Cambridge · GBUniversity of Oslo · NOMaastricht University · NLNorwegian University of Science and Technology · NO

Funding

British Heart Foundation CH/2000003/12800British Heart Foundation CH2000003/12800British Heart Foundation PG/16/11/32021British Heart Foundation PG/19/6/34153British Heart Foundation RG/08/009/25841British Heart Foundation RG/13/14/30314British Heart Foundation RG/20/2/34763
6 · The paper itself

Abstract

BACKGROUND AND

aimsAtherogenesis involves a complex interaction between immune cells and lipids, processes greatly influenced by the vascular smooth muscle cell (VSMC) phenotype. The DNA glycosylase NEIL3 has previously been shown to have a role in atherogenesis, though whether this is due to its ability to repair DNA damage or to other non-canonical functions is not yet clear. Hereby, we investigate the role of NEIL3 in atherogenesis, specifically in VSMC phenotypic modulation, which is critical in plaque formation and stability.

methodsChow diet-fed atherosclerosis-prone Apoe

resultsWe show that Neil3 deficiency increases atherosclerotic plaque development without affecting systemic lipids. This observation was associated with a shift in VSMC phenotype towards a proliferating, lipid-accumulating and secretory macrophage-like cell phenotype, without changes in DNA damage. VSMC transdifferentiation in Neil3-deficient mice encompassed increased activity of the Akt signaling pathway, supported by cell experiments showing Akt-dependent proliferation in NEIL3-abrogated human primary aortic VSMCs.

conclusionsOur findings show that Neil3 deficiency promotes atherosclerosis development through non-canonical mechanisms affecting VSMC phenotype involving activation of the Akt signaling pathway.

Indexed as

AtherosclerosisDNA GlycosylasesPlaque, AtheroscleroticAnimalsCell ProliferationCells, CulturedEndodeoxyribonucleasesHumansMiceMice, Inbred C57BLMice, Knockout, ApoEMuscle, Smooth, VascularMyocytes, Smooth MuscleN-Glycosyl HydrolasesPhenotypeDNA GlycosylasesEndodeoxyribonucleasesNEIL3 protein, humanNEIL3 protein, mouseN-Glycosyl HydrolasesAkt signalingAtherosclerosisDNA damage repairNEIL3Phenotypic transdifferentiationVascular smooth muscle cells

Identifiers

PMID33714552
OpenAlexW3129421182

What OpenQuestion holds

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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.