Evidence map›Paper›PMID 24972372›Full record

ArticleMolecular pharmaceutics2014

Amphiphilic nanoparticles repress macrophage atherogenesis: novel core/shell designs for scavenger receptor targeting and down-regulation.

Latrisha K Petersen, Adam W York, Daniel R Lewis, Sonali Ahuja, Kathryn E Uhrich, Robert K Prud'homme, Prabhas V Moghe

Abstract read
In one paragraph

Article in Molecular pharmaceutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.1field-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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Nanomedicines for dysfunctional macrophage-associated diseases.Journal of controlled release : official journal of the Controlled Release Society · 2017
    Review
  13. Review
  14. Article
  15. Article
  16. Designing polymers with sugar-based advantages for bioactive delivery applications.Journal of controlled release : official journal of the Controlled Release Society · 2015
    Review
  17. Sugar-based amphiphilic nanoparticles arrest atherosclerosis in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  18. Article
  19. Article
  20. 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

7 authors at 2 institutions in 1 country.

Latrisha K PetersenDepartment of Biomedical Engineering, Rutgers University , 599 Taylor Road, Piscataway, New Jersey 08854, United States.
Adam W York
Daniel R Lewis
Sonali Ahuja
Kathryn E Uhrich
Robert K Prud'homme
Prabhas V Moghe
Rutgers, The State University of New Jersey · USPrinceton University · US

Funding

UMDNJ TRAINING GRANT IN BIOTECHNOLOGYT32GM008339 · NIGMS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI YARMUSH, MARTIN L · 1989 to 2019
$6.1M
Translational Research in Regenerative MedicineT32EB005583 · NIBIB · RUTGERS, THE STATE UNIV OF N.J. · PI LEE, KIBUM, PAREKKADAN, BIJU · 2006 to 2022
$4.7M
Synthetic Counter-ligands for Inhibition of AtherosclerosisR01HL107913 · NHLBI · RUTGERS, THE STATE UNIV OF N.J. · PI MOGHE, PRABHAS V, UHRICH, KATHRYN ELIZABETH · 2011 to 2014
$2.3M
Nanoscale Receptor Blockers for Inhibition of AtherosclerosisR21HL093753 · NHLBI · RUTGERS, THE STATE UNIV OF N.J. · PI MOGHE, PRABHAS V · 2009 to 2010
$671k
NHLBI NIH HHS R01 HL107913NHLBI NIH HHS R01HL107913NHLBI NIH HHS R21 HL093753NHLBI NIH HHS R21HL93753NIBIB NIH HHS EB005583NIBIB NIH HHS T32 EB005583NIGMS NIH HHS T32 GM008339NIGMS NIH HHS T32GM008339
6 · The paper itself

Abstract

Atherosclerosis, an inflammatory lipid-rich plaque disease is perpetuated by the unregulated scavenger-receptor-mediated uptake of oxidized lipoproteins (oxLDL) in macrophages. Current treatments lack the ability to directly inhibit oxLDL accumulation and foam cell conversion within diseased arteries. In this work, we harness nanotechnology to design and fabricate a new class of nanoparticles (NPs) based on hydrophobic mucic acid cores and amphiphilic shells with the ability to inhibit the uncontrolled uptake of modified lipids in human macrophages. Our results indicate that tailored NP core and shell formulations repress oxLDL internalization via dual complementary mechanisms. Specifically, the most atheroprotective molecules in the NP cores competitively reduced NP-mediated uptake to scavenger receptor A (SRA) and also down-regulated the surface expression of SRA and CD36. Thus, nanoparticles can be designed to switch activated, lipid-scavenging macrophages to antiatherogenic phenotypes, which could be the basis for future antiatherosclerotic therapeutics.

Indexed as

AtherosclerosisArteriosclerosisCD36 AntigensDown-RegulationFoam CellsGene Expression RegulationHumansInflammationLeukocytes, MononuclearLipid MetabolismLipoproteinsLipoproteins, LDLMacrophagesNanoparticlesNanotechnologyPhenotypeCD36 AntigensLipoproteinsLipoproteins, LDLoxidized low density lipoproteinScavenger Receptors, Class A

Identifiers

PMID24972372
PMCPMC4144725
OpenAlexW2334855861

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.