Evidence map›Paper›PMID 28912717›Full record

ArticleFrontiers in pharmacology2017

Global Metabolomics Reveals the Metabolic Dysfunction in Ox-LDL Induced Macrophage-Derived Foam Cells.

Wenjuan Xu, Ziyi Wei, Jiaojiao Dong, Feipeng Duan, Kuikui Chen, Chang Chen, Jie Liu, Xiaowei Yang, Lianming Chen, Hongbin Xiao and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

8 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Integrated Metabolomics and Network Pharmacology Study on Immunoregulation Mechanisms ofEvidence-based complementary and alternative medicine : eCAM · 2019
    Article
  8. 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

11 authors at 2 institutions in 1 country.

Wenjuan XuInstitute of Chinese Materia Medica, China Academy of Chinese Medical SciencesBeijing, China.
Ziyi WeiSchool of Chinese Materia Medica, Beijing University of Chinese MedicineBeijing, China.
Jiaojiao DongSchool of Chinese Materia Medica, Beijing University of Chinese MedicineBeijing, China.
Feipeng DuanSchool of Chinese Materia Medica, Beijing University of Chinese MedicineBeijing, China.
Kuikui ChenSchool of Chinese Materia Medica, Beijing University of Chinese MedicineBeijing, China.
Chang ChenInstitute of Chinese Materia Medica, China Academy of Chinese Medical SciencesBeijing, China.
Jie LiuSchool of Chinese Materia Medica, Beijing University of Chinese MedicineBeijing, China.
Xiaowei YangInstitute of Chinese Materia Medica, China Academy of Chinese Medical SciencesBeijing, China.
Lianming ChenSchool of Chinese Materia Medica, Beijing University of Chinese MedicineBeijing, China.
Hongbin XiaoSchool of Chinese Materia Medica, Beijing University of Chinese MedicineBeijing, China.
An LiuInstitute of Chinese Materia Medica, China Academy of Chinese Medical SciencesBeijing, China.
Beijing University of Chinese Medicine · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis (AS) is a chronic disorder of large arteries that is a major risk factors of high morbidity and mortality. Oxidative modification LDL is one of the important contributors to atherogenesis. Macrophages take up ox-LDL and convert into foam cells, which is the hallmark of AS. To advance the understanding of the metabolic perturbation involved in ox-LDL induced macrophage-derived foam cells and discover the potential biomarkers of early AS, a global metabolomics approach was applied based on UHPLC-QTOF/MS. Multivariate statistical analyses identified five metabolites (25-azacholesterol, anandamide, glycocholate, oleoyl ethanolamide, and 3-oxo-4, 6-choladienoate) for distinguishing foamy macrophages from controls. Among the six main metabolic pathways, the unsaturated fatty acid, especially arachidonic acid metabolism, contributed importantly to early AS. A new biomarker, anandamide (AEA), whose synthesis and metabolism in macrophages are disturbed by overloaded ox-LDL, results in metabolic obstruction. This study is the first to investigate the metabolic disturbance in macrophage-derived foam cells induced by ox-LDL and screen potential biomarkers and metabolic pathways associated with early AS. Our findings provide a new insight in the underlying pathophysiological mechanisms and also help to identify novel targets for the intervention of AS.

Indexed as

anandamide over-accumulationatherosclerosismacrophage-derived foam cellsmetabolomicsoxidized-LDL

Identifiers

PMID28912717
PMCPMC5583968
OpenAlexW2753442708

What OpenQuestion holds

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LicenceCC BY
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.