Evidence map›Paper›PMID 27040361›Full record

ArticleJournal of atherosclerosis and thrombosis2016

Iron Together with Lipid Downregulates Protein Levels of Ceruloplasmin in Macrophages Associated with Rapid Foam Cell Formation.

Qi Wang, Jiajie Ji, Shuangying Hao, Meng Zhang, Kuanyu Li, Tong Qiao

Open access · diamondAbstract read
In one paragraph

Article in Journal of atherosclerosis and thrombosis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 29 citations in OpenAlex.

  1. MLK3 promotes atherosclerosis by regulating ferroptosis in macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  2. Article
  3. Ironing out macrophages in atherosclerosis.Acta biochimica et biophysica Sinica · 2023
    Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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

6 authors at 3 institutions in 1 country.

Qi WangDepartment of Vascular Surgery, Drum Tower Clinical Medical College of Nanjing Medical University.
Jiajie Ji
Shuangying Hao
Meng Zhang
Kuanyu Li
Tong Qiao
Nanjing Drum Tower Hospital · CNNanjing Medical University · CNNanjing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimIron accumulation in foam cells was previously shown to be involved in atherogenesis. However, the mechanism for iron accumulation was not clarified. Ceruloplasmin (Cp) is an important factor in cellular iron efflux and was found to be downregulated in atherosclerotic plaques in our previous study. The current study is to investigate the role of Cp in atherosclerosis.

methodsWe used RAW264.7 cells, a well-accepted cell model of atherosclerosis, which were treated with lipopolysaccharides (LPS), ferric ammonium citrate (FAC) or deferoxamine, and oxidized low density lipoprotein (ox-LDL) to detect the regulation of Cp and its influence in iron efflux and lipid accumulation using biochemical and histological assays.

resultsOur results showed that the Cp protein level increased after 200-μM FAC treatment in LPS-activated RAW264.7 cells. Ox-LDL treatment (50 μg/ml) moderately reduced both mRNA and protein levels and ferroxidase activity of Cp (p<0.05). No significant difference was observed in the expression of ferritin and ferroportin, two important iron-related proteins for iron storage and efflux, respectively, after ox-LDL treatment. However, co-treatment with ox-LDL and FAC drastically reduced the expression of Cp. Accordingly, the ferroxidase activities simultaneously decreased, whereas the protein levels of Ft and Fpn1 significantly increased, indicating further iron accumulation. Moreover, co-treatment with FAC and ox-LDL enhanced the accumulation of cholesterol compared with ox-LDL-only treatment to trigger apoptosis.

conclusionOur findings suggest that physiological interaction of iron and lipid obstructs iron efflux and accelerates the lipid accumulation in macrophages during foam cell formation, which implicates the role of iron in the pathology of atherosclerosis.

Indexed as

AtherosclerosisBlotting, WesternCells, CulturedCeruloplasminDown-RegulationFlow CytometryFoam CellsGene Expression RegulationHumansIronLipidsMacrophagesReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerCeruloplasminIronLipidsRNA, Messenger

Identifiers

PMID27040361
PMCPMC5098920
OpenAlexW2312436405

What OpenQuestion holds

Textmetadata
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.