Evidence map›Paper›PMID 20491656›Full record

ArticleClinical science (London, England : 1979)2010

Overexpression of STARD3 in human monocyte/macrophages induces an anti-atherogenic lipid phenotype.

Faye Borthwick, Anne-Marie Allen, Janice M Taylor, Annette Graham

Open access · hybridAbstract read
In one paragraph

Article in Clinical science (London, England : 1979), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.3field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
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  15. Insights into the mechanisms of sterol transport between organelles.Cellular and molecular life sciences : CMLS · 2013
    Review
  16. Article
  17. Article
  18. Genetics of cholesterol efflux.Current atherosclerosis reports · 2012
    Review
  19. 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

4 authors at 1 institution in 1 country.

Faye BorthwickVascular Biology Group, Department of Biological and Biomedical Sciences, Glasgow Caledonian University, Glasgow G4 0BA, UK.
Anne-Marie Allen
Janice M Taylor
Annette Graham
Glasgow Caledonian University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulated macrophage cholesterol homoeostasis lies at the heart of early and developing atheroma, and removal of excess cholesterol from macrophage foam cells, by efficient transport mechanisms, is central to stabilization and regression of atherosclerotic lesions. The present study demonstrates that transient overexpression of STARD3 {START [StAR (steroidogenic acute regulatory protein)-related lipid transfer] domain 3; also known as MLN64 (metastatic lymph node 64)}, an endosomal cholesterol transporter and member of the 'START' family of lipid trafficking proteins, induces significant increases in macrophage ABCA1 (ATP-binding cassette transporter A1) mRNA and protein, enhances [(3)H]cholesterol efflux to apo (apolipoprotein) AI, and reduces biosynthesis of cholesterol, cholesteryl ester, fatty acids, triacylglycerol and phospholipids from [(14)C]acetate, compared with controls. Notably, overexpression of STARD3 prevents increases in cholesterol esterification in response to acetylated LDL (low-density lipoprotein), blocking cholesteryl ester deposition. Thus enhanced endosomal trafficking via STARD3 induces an anti-atherogenic macrophage lipid phenotype, positing a potentially therapeutic strategy.

Indexed as

AortaAtherosclerosisCarrier ProteinsCells, CulturedFoam CellsGene Expression RegulationHumansLipid MetabolismMacrophagesMembrane ProteinsMonocytesPhenotypePolymerase Chain ReactionRNA, MessengerCarrier ProteinsMembrane ProteinsRNA, MessengerSTARD3 protein, human

Identifiers

PMID20491656
PMCPMC2891001
OpenAlexW2036726452

What OpenQuestion holds

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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.