Evidence map›Paper›PMID 16075060›Full record

ArticleThe Journal of clinical investigation2005

Loss of receptor-mediated lipid uptake via scavenger receptor A or CD36 pathways does not ameliorate atherosclerosis in hyperlipidemic mice.

Kathryn J Moore, Vidya V Kunjathoor, Stephanie L Koehn, Jennifer J Manning, Anita A Tseng, Jessica M Silver, Mary McKee, Mason W Freeman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
170citing papers in PubMed, 1 pooled it
9.1field-weighted citation impact, top 1% 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

170 citing papers in PubMed, 1 synthesis or guideline pooled it, 377 citations in OpenAlex.

  1. Impacts ofCardiovascular therapeutics · 2025
    Pooled it
  2. Sphingolipids and Atherosclerosis.Current atherosclerosis reports · 2026
    Review
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  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Unbalanced Redox With Autophagy in Cardiovascular Disease.Journal of lipid and atherosclerosis · 2023
    Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

110 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Kathryn J MooreLipid Metabolism Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.
Vidya V Kunjathoor
Stephanie L Koehn
Jennifer J Manning
Anita A Tseng
Jessica M Silver
Mary McKee
Mason W Freeman
Centre de recherche Translationnelle en Médecine moléculaire · FRHarvard University · US

Funding

Mechanisms of CD36 Signal TransductionR01AG020255 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI MOORE, KATHRYN J · 2001 to 2011
$3.7M
REGULATION OF SCAVENGER RECEPTORS IN ATHEROSCLEROSISR01HL045098 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI FREEMAN, MASON W · 1990 to 2003
$1.7M
NHLBI NIH HHS HL45098NHLBI NIH HHS R01 HL045098NIA NIH HHS AG20255NIA NIH HHS R01 AG020255
6 · The paper itself

Abstract

Macrophage internalization of modified lipoproteins is thought to play a critical role in the initiation of atherogenesis. Two scavenger receptors, scavenger receptor A (SR-A) and CD36, have been centrally implicated in this lipid uptake process. Previous studies showed that these receptors mediated the majority of cholesterol ester accumulation in macrophages exposed to oxidized LDL and that mice with deletions of either receptor exhibited marked reductions in atherosclerosis. This work has contributed to an atherosclerosis paradigm: scavenger receptor-mediated oxidized lipoprotein uptake is required for foam cell formation and atherogenesis. In this study, Apoe-/- mice lacking SR-A or CD36, backcrossed into the C57BL/6 strain for 7 generations, were fed an atherogenic diet for 8 weeks. Hyperlipidemic Cd36-/-Apoe-/- and Msr1-/-Apoe-/- mice showed significant reductions in peritoneal macrophage lipid accumulation in vivo; however, in contrast with previous reports, this was associated with increased aortic sinus lesion areas. Characterization of aortic sinus lesions by electron microscopy and immunohistochemistry showed abundant macrophage foam cells, indicating that lipid uptake by intimal macrophages occurs in the absence of CD36 or SR-A. These data show that alternative lipid uptake mechanisms may contribute to macrophage cholesterol ester accumulation in vivo and suggest that the roles of SR-A and CD36 as proatherosclerotic mediators of modified LDL uptake in vivo need to be reassessed.

Indexed as

AnimalsApolipoproteins EArteriosclerosisCD36 AntigensCholesterol EstersDiet, AtherogenicFoam CellsHyperlipidemiasLipoproteins, LDLMacrophages, PeritonealMiceMice, KnockoutReceptors, ImmunologicReceptors, ScavengerScavenger Receptors, Class ASinus of ValsalvaApolipoproteins ECD36 AntigensCholesterol EstersLipoproteins, LDLMsr1 protein, mouseoxidized low density lipoproteinReceptors, ImmunologicReceptors, ScavengerScavenger Receptors, Class A

Identifiers

PMID16075060
PMCPMC1180534
OpenAlexW2115017173

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.