Evidence map›Paper›PMID 29880490›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2018

Acute Loss of Apolipoprotein E Triggers an Autoimmune Response That Accelerates Atherosclerosis.

Monica Centa, Kajsa E Prokopec, Manasa G Garimella, Katrin Habir, Lisa Hofste, Julian M Stark, Albert Dahdah, Chris A Tibbitt, Konstantinos A Polyzos, Anton Gisterå and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
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  3. CD80Cell communication and signaling : CCS · 2026
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  19. Apolipoprotein E and Atherosclerosis.Current atherosclerosis reports · 2021
    Review
  20. Article
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

18 authors at 4 institutions in 3 countries.

Monica CentaFrom the Department of Medicine and Center for Molecular Medicine, Karolinska University Hospital (M.C., K.E.P., K.H., L.H., A.D., K.A.P., A.G., D.K.J., G.K.H., D.F.J.K., S.M.).
Kajsa E ProkopecFrom the Department of Medicine and Center for Molecular Medicine, Karolinska University Hospital (M.C., K.E.P., K.H., L.H., A.D., K.A.P., A.G., D.K.J., G.K.H., D.F.J.K., S.M.).
Manasa G GarimellaDepartment of Microbiology, Tumor, and Cell Biology (M.G.G., J.M.S., C.A.T., J.M.C., M.C.I.K.), Karolinska Institutet, Stockholm, Sweden.
Katrin HabirFrom the Department of Medicine and Center for Molecular Medicine, Karolinska University Hospital (M.C., K.E.P., K.H., L.H., A.D., K.A.P., A.G., D.K.J., G.K.H., D.F.J.K., S.M.).
Lisa HofsteFrom the Department of Medicine and Center for Molecular Medicine, Karolinska University Hospital (M.C., K.E.P., K.H., L.H., A.D., K.A.P., A.G., D.K.J., G.K.H., D.F.J.K., S.M.).
Julian M StarkDepartment of Microbiology, Tumor, and Cell Biology (M.G.G., J.M.S., C.A.T., J.M.C., M.C.I.K.), Karolinska Institutet, Stockholm, Sweden.
Albert DahdahFrom the Department of Medicine and Center for Molecular Medicine, Karolinska University Hospital (M.C., K.E.P., K.H., L.H., A.D., K.A.P., A.G., D.K.J., G.K.H., D.F.J.K., S.M.).
Chris A TibbittDepartment of Microbiology, Tumor, and Cell Biology (M.G.G., J.M.S., C.A.T., J.M.C., M.C.I.K.), Karolinska Institutet, Stockholm, Sweden.
Konstantinos A PolyzosFrom the Department of Medicine and Center for Molecular Medicine, Karolinska University Hospital (M.C., K.E.P., K.H., L.H., A.D., K.A.P., A.G., D.K.J., G.K.H., D.F.J.K., S.M.).
Anton GisteråFrom the Department of Medicine and Center for Molecular Medicine, Karolinska University Hospital (M.C., K.E.P., K.H., L.H., A.D., K.A.P., A.G., D.K.J., G.K.H., D.F.J.K., S.M.).
Daniel K JohanssonFrom the Department of Medicine and Center for Molecular Medicine, Karolinska University Hospital (M.C., K.E.P., K.H., L.H., A.D., K.A.P., A.G., D.K.J., G.K.H., D.F.J.K., S.M.).
Nobuyo N MaedaDepartment of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill (N.N.M.).
Göran K HanssonFrom the Department of Medicine and Center for Molecular Medicine, Karolinska University Hospital (M.C., K.E.P., K.H., L.H., A.D., K.A.P., A.G., D.K.J., G.K.H., D.F.J.K., S.M.).
Daniel F J KetelhuthFrom the Department of Medicine and Center for Molecular Medicine, Karolinska University Hospital (M.C., K.E.P., K.H., L.H., A.D., K.A.P., A.G., D.K.J., G.K.H., D.F.J.K., S.M.).
Jonathan M CoquetDepartment of Microbiology, Tumor, and Cell Biology (M.G.G., J.M.S., C.A.T., J.M.C., M.C.I.K.), Karolinska Institutet, Stockholm, Sweden.
Christoph J BinderDepartment of Laboratory Medicine, Medical University of Vienna, Austria (C.J.B.).
Mikael C I KarlssonDepartment of Microbiology, Tumor, and Cell Biology (M.G.G., J.M.S., C.A.T., J.M.C., M.C.I.K.), Karolinska Institutet, Stockholm, Sweden.
Stephen MalinFrom the Department of Medicine and Center for Molecular Medicine, Karolinska University Hospital (M.C., K.E.P., K.H., L.H., A.D., K.A.P., A.G., D.K.J., G.K.H., D.F.J.K., S.M.).
Karolinska University Hospital · SEKarolinska Institutet · SECeMM Research Center for Molecular Medicine · ATUniversity of North Carolina at Chapel Hill · US

Funding

MODELS FOR STUDYING THE GENETICS OF HYPERTENSIONR01HL049277 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MAEDA, NOBUYO · 1992 to 2025
$17.5M
APOLIPOROTEIN GENES AND ATHEROGENESISR01HL042630 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MAEDA, NOBUYO · 1989 to 2017
$4.9M
Austrian Science Fund FWF F 3015Austrian Science Fund FWF F 5402NHLBI NIH HHS R01 HL042630NHLBI NIH HHS R01 HL049277
6 · The paper itself

Abstract

Objective- Dyslipidemia is a component of the metabolic syndrome, an established risk factor for atherosclerotic cardiovascular disease, and is also observed in various autoimmune and chronic inflammatory conditions. However, there are limited opportunities to study the impact of acquired dyslipidemia on cardiovascular and immune pathology. Approach and Results- We designed a model system that allows for the conversion to a state of acute hyperlipidemia in adult life, so that the consequences of such a transition could be observed, through conditionally deleting APOE (apolipoprotein E) in the adult mouse. The transition to hypercholesterolemia was accompanied by adaptive immune responses, including the expansion of T lymphocyte helper cell 1, T follicular helper cell, and T regulatory subsets and the formation of germinal centers. Unlike steady-state Apoe

Indexed as

Adaptive ImmunityAutoimmunityAnimalsAortaAortic DiseasesApolipoproteins EAtherosclerosisB-LymphocytesCells, CulturedDisease Models, AnimalDisease ProgressionDyslipidemiasGerminal CenterImmunity, HumoralInflammationMice, Inbred C57BLApolipoproteins Eapolipoproteins Eatherosclerosishyperlipidemiasinflammationmetabolic syndrome

Identifiers

PMID29880490
PMCPMC6173285
OpenAlexW2806403717

What OpenQuestion holds

Textmetadata
LicenceTDM
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.