Evidence map›Paper›PMID 32790236›Full record

ArticleImmunity, inflammation and disease2020

Аtherosclerosis-like changes in the rabbit aortic wall induced by immunization with native high-density lipoproteins.

Kseniya Fomina, Liubov Beduleva, Igor Menshikov, Abdulkadhim Zerjawi, Alexey Terentiev, Alexandr Sidorov, Tatyana Khramova, Nadezhda Abisheva, Anna Gorbushina

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 51% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. 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

9 authors at 2 institutions in 1 country.

Kseniya FominaLaboratory of Molecular and Cell Immunology, Department of Immunology and Cell Biology, Udmurt State University, Izhevsk, Russian Federation.
Liubov BedulevaLaboratory of Molecular and Cell Immunology, Department of Immunology and Cell Biology, Udmurt State University, Izhevsk, Russian Federation.ORCID 0000-0002-2515-5960
Igor MenshikovLaboratory of Molecular and Cell Immunology, Department of Immunology and Cell Biology, Udmurt State University, Izhevsk, Russian Federation.
Abdulkadhim ZerjawiLaboratory of Molecular and Cell Immunology, Department of Immunology and Cell Biology, Udmurt State University, Izhevsk, Russian Federation.
Alexey TerentievLaboratory of Molecular and Cell Immunology, Department of Immunology and Cell Biology, Udmurt State University, Izhevsk, Russian Federation.
Alexandr SidorovLaboratory of Molecular and Cell Immunology, Department of Immunology and Cell Biology, Udmurt State University, Izhevsk, Russian Federation.
Tatyana KhramovaLaboratory of Molecular and Cell Immunology, Department of Immunology and Cell Biology, Udmurt State University, Izhevsk, Russian Federation.
Nadezhda AbishevaLaboratory of Molecular and Cell Immunology, Department of Immunology and Cell Biology, Udmurt State University, Izhevsk, Russian Federation.
Anna GorbushinaLaboratory of Molecular and Cell Immunology, Department of Immunology and Cell Biology, Udmurt State University, Izhevsk, Russian Federation.
Udmurt Federal Research Center, Ural Branch of the Russian Academy of Sciences · RUUdmurt State University · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionA high level of total cholesterol or low-density lipoprotein (LDL) cholesterol is considered the main cause of atherosclerosis and cardiovascular disease. For this reason, experimental atherosclerosis is induced by creating high blood cholesterol in animals. However, the hypothesis that atherosclerotic processes are mostly caused by immune (autoimmune) mechanisms has recently been gaining traction. At the same time, no experimental model has been developed that clearly demonstrates the autoimmune mechanism by which atherosclerosis develops and reproduces the full picture of atherosclerosis solely by means of an immune response, without resorting to additional interventions such as a high-cholesterol diet or the use of genetic models of hyperlipidemia. Previously, we were able to induce atherosclerosis-like lesions in the aorta and the development of pericardial fat in rats by immunizing them with human native lipoproteins. The purpose of this study was to test whether atherosclerosis can be induced in normocholesterolaemic rabbits by immunizing them with human native high-density lipoproteins (hnHDL).

methodsRabbits were immunized with hnHDL. Aortic wall structure, plasma cholesterol level, and antibodies against HDL were studied.

resultsImmunization with hnHDL was found to cause atherosclerosis-like lesions in the rabbit aorta such as adipocytic and chondrocytic metaplasia, proteoglycan deposits, leukocytic infiltration. Atherosclerosis-like lesions developed in the aorta of hnHDL-immunized rabbits against a background of normal blood LDL-cholesterol level. Therefore, a high plasma cholesterol level is not the sole cause of atherosclerosis. The immune response against HDL is an independent cause of atherogenesis.

conclusionsA rabbit model of atherosclerosis caused by immunization with hnHDL can be widely used to examine the mechanisms occurring during atherogenesis.

Indexed as

AtherosclerosisAnimalsAortaImmunizationLipoproteins, HDLLipoproteins, LDLMaleRabbitsRatsLipoproteins, HDLLipoproteins, LDLantibodies specific to HDLaortic wall metaplasiaatherosclerosischolesterolchondrocyte-like cells

Identifiers

PMID32790236
PMCPMC7654427
OpenAlexW3048960570

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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.