Evidence map›Paper›PMID 24466087›Full record

ArticlePloS one2014

Increased metabolite levels of glycolysis and pentose phosphate pathway in rabbit atherosclerotic arteries and hypoxic macrophage.

Atsushi Yamashita, Yan Zhao, Yunosuke Matsuura, Kazuaki Yamasaki, Sayaka Moriguchi-Goto, Chihiro Sugita, Takashi Iwakiri, Nozomi Okuyama, Chihiro Koshimoto, Keiichi Kawai and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.6field-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

31 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
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  7. Advances in Glycolysis Metabolism of Atherosclerosis.Journal of cardiovascular translational research · 2023
    Review
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  13. Atherosclerosis Impairs Naive CD4 T-Cell Responses via Disruption of Glycolysis.Arteriosclerosis, thrombosis, and vascular biology · 2021
    Article
  14. Article
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  16. A longitudinalCardiovascular diagnosis and therapy · 2021
    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

14 authors at 4 institutions in 1 country.

Atsushi YamashitaDepartment of Pathology, University of Miyazaki, Miyazaki, Japan.
Yan ZhaoDepartment of Tracer Kinetics & Bioanalysis, Hokkaido University, Sapporo, Japan.
Yunosuke MatsuuraDepartment of Pathology, University of Miyazaki, Miyazaki, Japan ; Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Kazuaki YamasakiDepartment of Tracer Kinetics & Bioanalysis, Hokkaido University, Sapporo, Japan.
Sayaka Moriguchi-GotoDepartment of Pathology, University of Miyazaki, Miyazaki, Japan.
Chihiro SugitaDepartment of Pathology, University of Miyazaki, Miyazaki, Japan.
Takashi IwakiriDepartment of Pathology, University of Miyazaki, Miyazaki, Japan ; Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Nozomi OkuyamaDepartment of Pathology, University of Miyazaki, Miyazaki, Japan.
Chihiro KoshimotoFrontier Science Research Center, University of Miyazaki, Miyazaki, Japan.
Keiichi KawaiFaculty of Health Sciences, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Ishikawa, Japan ; Biomedical Imaging Research Center, University of Fukui, Fukui, Japan.
Nagara TamakiDepartment of Nuclear Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Songji ZhaoDepartment of Tracer Kinetics & Bioanalysis, Hokkaido University, Sapporo, Japan.
Yuji KugeCentral Institute of Isotope Science, Hokkaido University, Sapporo, Japan.
Yujiro AsadaDepartment of Pathology, University of Miyazaki, Miyazaki, Japan.
University of Miyazaki · JPHokkaido University · JPHokkaido University of Science · JPUniversity of Fukui · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsInflammation and possibly hypoxia largely affect glucose utilization in atherosclerotic arteries, which could alter many metabolic systems. However, metabolic changes in atherosclerotic plaques remain unknown. The present study aims to identify changes in metabolic systems relative to glucose uptake and hypoxia in rabbit atherosclerotic arteries and cultured macrophages.

methodsMacrophage-rich or smooth muscle cell (SMC)-rich neointima was created by balloon injury in the iliac-femoral arteries of rabbits fed with a 0.5% cholesterol diet or a conventional diet. THP-1 macrophages stimulated with lipopolysaccharides (LPS) and interferon-γ (INFγ) were cultured under normoxic and hypoxic conditions. We evaluated comprehensive arterial and macrophage metabolism by performing metabolomic analyses using capillary electrophoresis-time of flight mass spectrometry. We evaluated glucose uptake and its relationship to vascular hypoxia using (18)F-fluorodeoxyglucose ((18)F-FDG) and pimonidazole, a marker of hypoxia.

resultsThe levels of many metabolites increased in the iliac-femoral arteries with macrophage-rich neointima, compared with those that were not injured and those with SMC-rich neointima (glycolysis, 4 of 9; pentose phosphate pathway, 4 of 6; tricarboxylic acid cycle, 4 of 6; nucleotides, 10 of 20). The uptake of (18)F-FDG in arterial walls measured by autoradiography positively correlated with macrophage- and pimonidazole-immunopositive areas (r = 0.76, and r = 0.59 respectively; n = 69 for both; p<0.0001). Pimonidazole immunoreactivity was closely localized with the nuclear translocation of hypoxia inducible factor-1α and hexokinase II expression in macrophage-rich neointima. The levels of glycolytic (8 of 8) and pentose phosphate pathway (4 of 6) metabolites increased in LPS and INFγ stimulated macrophages under hypoxic but not normoxic condition. Plasminogen activator inhibitor-1 protein levels in the supernatant were closely associated with metabolic pathways in the macrophages.

conclusionInfiltrative macrophages in atherosclerotic arteries might affect metabolic systems, and hypoxia but not classical activation might augment glycolytic and pentose phosphate pathways in macrophages.

Indexed as

GlycolysisPentose Phosphate PathwayActive Transport, Cell NucleusAnimalsAtherosclerosisCell HypoxiaCell LineFemoral ArteryFluorodeoxyglucose F18HumansHypoxia-Inducible Factor 1, alpha SubunitMacrophagesMaleMetabolomeRabbitsRadionuclide ImagingFluorodeoxyglucose F18Hypoxia-Inducible Factor 1, alpha SubunitRadiopharmaceuticalsThromboplastin

Identifiers

PMID24466087
PMCPMC3900532
OpenAlexW2025834965

What OpenQuestion holds

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LicenceCC BY
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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.