Evidence map›Paper›PMID 30205792›Full record

ArticleCurrent pharmaceutical design2018

Modified LDL Particles Activate Inflammatory Pathways in Monocyte-derived Macrophages: Transcriptome Analysis.

Alexander N Orekhov, Yumiko Oishi, Nikita G Nikiforov, Andrey V Zhelankin, Larisa Dubrovsky, Igor A Sobenin, Alexander Kel, Daria Stelmashenko, Vsevolod J Makeev, Kathy Foxx and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Current pharmaceutical design, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

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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

13 authors at 7 institutions in 3 countries.

Alexander N OrekhovLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russian Federation.
Yumiko OishiDepartment of Cellular and Molecular Medicine, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 1138510, Japan.
Nikita G NikiforovLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russian Federation.
Andrey V ZhelankinLaboratory of postgenomic research, Federal Research and Clinical Center of Physical-Chemical Medicine, 119435 Moscow, Russian Federation.
Larisa DubrovskyGW School of Medicine and Health Sciences, George Washington University, Washington, DC 20037, United States.
Igor A SobeninLaboratory of Medical Genetics, Institute of Experimental Cardiology, National Medical Research Center of Cardiology, 121552 Moscow, Russian Federation.
Alexander KelBiosoft.ru Ltd, 630001 Novosibirsk, Russian Federation.
Daria StelmashenkoBiosoft.ru Ltd, 630001 Novosibirsk, Russian Federation.
Vsevolod J MakeevVavilov Institute of General Genetics, Russian Academy of Sciences, Moscow 119991, Russian Federation.
Kathy FoxxKalen Biomedical, LLC, Montgomery Village, MD 20886, United States.
Xueting JinExperimental Atherosclerosis Section, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, United States.
Howard S KruthExperimental Atherosclerosis Section, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, United States.
Michael BukrinskyGW School of Medicine and Health Sciences, George Washington University, Washington, DC 20037, United States.
George Washington University · USNational Institutes of Health · USResearch Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences · RUInstitute of Experimental Cardiology · RUResearch Institute of Physical Chemical Medicine · RUTokyo Medical and Dental University · JPVavilov Institute of General Genetics · RU

Funding

Mechanism Of Cholesterol Accumulation In Human AtherosclerosisZIAHL002832 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI KRUTH, HOWARD S · 2009 to 2019
$12.3M
The District of Columbia Developmental Center for AIDS Research (DC D-CFAR)P30AI087714 · NIAID · GEORGE WASHINGTON UNIVERSITY · PI GREENBERG, ALAN EDWARD · 2010 to 2014
$8.4M
HIV Disease and Impairement of High Density Lipoprotein MetabolismR01HL101274 · NHLBI · GEORGE WASHINGTON UNIVERSITY · PI BUKRINSKY, MICHAEL ILYA, FITZGERALD, MICHAEL LEO · 2010 to 2015
$4.0M
Metabolic complications of HIV disease caused by Nef released from HIV-infected cellsR01HL131473 · NHLBI · GEORGE WASHINGTON UNIVERSITY · PI BUKRINSKY, MICHAEL ILYA, SVIRIDOV, DMITRI · 2016 to 2019
$1.6M
NHLBI NIH HHS R01 HL101274NHLBI NIH HHS R01 HL131473NIAID NIH HHS P30 AI087714
6 · The paper itself

Abstract

backgroundA hallmark of atherosclerosis is its complex pathogenesis, which is dependent on altered cholesterol metabolism and inflammation. Both arms of pathogenesis involve myeloid cells. Monocytes migrating into the arterial walls interact with modified low-density lipoprotein (LDL) particles, accumulate cholesterol and convert into foam cells, which promote plaque formation and also contribute to inflammation by producing proinflammatory cytokines. A number of studies characterized transcriptomics of macrophages following interaction with modified LDL, and revealed alteration of the expression of genes responsible for inflammatory response and cholesterol metabolism. However, it is still unclear how these two processes are related to each other to contribute to atherosclerotic lesion formation.

methodsWe attempted to identify the main mater regulator genes in macrophages treated with atherogenic modified LDL using a bioinformatics approach.

resultsWe found that most of the identified genes were involved in inflammation, and none of them was implicated in cholesterol metabolism. Among the key identified genes were interleukin (IL)-7, IL-7 receptor, IL- 15 and CXCL8.

conclusionOur results indicate that activation of the inflammatory pathway is the primary response of the immune cells to modified LDL, while the lipid metabolism genes may be a secondary response triggered by inflammatory signalling.

Indexed as

Gene Expression ProfilingHealthy VolunteersHumansInflammationLipoproteins, LDLMacrophagesLipoproteins, LDLAtherosclerosisinflammationLDLmacrophagesmodified LDLpro-inflammatory signaling.

Identifiers

PMID30205792
PMCPMC6302360
OpenAlexW2891186478

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.