Evidence map›Paper›PMID 28124601›Full record

ReviewCurrent pharmaceutical design2017

Use of Primary Macrophages for Searching Novel Immunocorrectors.

Nikita G Nikiforov, Natalia V Elizova, Michael Bukrinsky, Larisa Dubrovsky, Vsevolod J Makeev, Yoshiyuki Wakabayashi, Poching Liu, Kathy K Foxx, Howard S Kruth, Xueting Jin and 2 more

Abstract readReview
In one paragraph

Review in Current pharmaceutical design, 2017. 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
0.1field-weighted citation impact, top 55% 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, 2 citations in OpenAlex.

  1. Article
  2. Trained Circulating Monocytes in Atherosclerosis:Frontiers in pharmacology · 2019
    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

12 authors at 6 institutions in 3 countries.

Nikita G NikiforovLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russian Federation.
Natalia V ElizovaLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russian Federation.
Michael BukrinskyGW School of Medicine and Health Sciences, George Washington University, 20037 Washington, DC, United States.
Larisa DubrovskyGW School of Medicine and Health Sciences, George Washington University, 20037 Washington, DC, United States.
Vsevolod J MakeevVavilov Institute of General Genetics, Russian Academy of Sciences, 119333 Moscow, Russian Federation.
Yoshiyuki WakabayashiDNA Sequencing and Genomics Core, National Heart, Lung, and Blood Institute, National Institutes of Health, 20892 Bethesda, MD, United States.
Poching LiuDNA Sequencing and Genomics Core, National Heart, Lung, and Blood Institute, National Institutes of Health, 20892 Bethesda, MD, United States.
Kathy K FoxxKalen Biomedical, LLC, 20886 Montgomery Village, MD, United States.
Howard S KruthExperimental Atherosclerosis Section, Center for Molecular, National Heart, Lung, and Blood Institute , National Institutes of Health, 20892 Bethesda, MD, United States.
Xueting JinExperimental Atherosclerosis Section, Center for Molecular, National Heart, Lung, and Blood Institute , National Institutes of Health, 20892 Bethesda, MD, United States.
Emile R ZakievINSERM UMR_S 1166, Faculte de Medecine Pitie-Salpetriere, University of Pierre and Marie Curie - Paris 6, 75013 Paris, France.
Alexander N OrekhovDepartment of Biophysics, Biological Faculty, Moscow State University, Moscow 119991, Russian Federation.
National Institutes of Health · USGeorge Washington University · USResearch Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences · RUInserm · FRLomonosov Moscow State University · RUVavilov 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
Intramural NIH HHS ZIA HL002832
6 · The paper itself

Abstract

In this mini-review, the role of macrophage phenotypes in atherogenesis is considered. Recent studies on distribution of M1 and M2 macrophages in different types of atherosclerotic lesions indicate that macrophages exhibit a high degree of plasticity of phenotype in response to various conditions in microenvironment. The effect of the accumulation of cholesterol, a key event in atherogenesis, on the macrophage phenotype is also discussed. The article presents the results of transcriptome analysis of cholesterol-loaded macrophages revealing genes involved in immune response whose expression rate has changed the most. It turned out that the interaction of macrophages with modified LDL leads to higher expression levels of pro-inflammatory marker TNF-α and antiinflammatory marker CCL18. Phenotypic profile of macrophage activation could be a good target for testing of novel anti-atherogenic immunocorrectors. A number of anti-atherogenic drugs were tested as potential immunocorrectors using primary macrophage-based model.

Indexed as

Adjuvants, ImmunologicAnimalsAnticholesteremic AgentsAtherosclerosisHumansMacrophagesAdjuvants, ImmunologicAnticholesteremic AgentsactivationAtherosclerosisimmunocorrectorsmacrophage-based testmacrophagesmodified LDLphenotypetranscriptome

Identifiers

PMID28124601
PMCPMC6446906
OpenAlexW2583940774

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.