Evidence map›Paper›PMID 10772649›Full record

ArticleThe Journal of clinical investigation2000

Targeted disruption of the class B scavenger receptor CD36 protects against atherosclerotic lesion development in mice.

M Febbraio, E A Podrez, J D Smith, D P Hajjar, S L Hazen, H F Hoff, K Sharma, R L Silverstein

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 377 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
377citing papers in PubMed, 1 pooled it
20.1field-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

377 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,035 citations in OpenAlex.

  1. Impacts ofCardiovascular therapeutics · 2025
    Pooled it
  2. Trial
  3. Article
  4. Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
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317 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 4 institutions in 1 country.

M FebbraioDepartment of Medicine, Division of Hematology and Medical Oncology, Center of Vascular Biology, Weill Medical College of Cornell University, New York, New York 10021, USA. mjfebbra@med.cornell.edu
E A Podrez
J D Smith
D P Hajjar
S L Hazen
H F Hoff
K Sharma
R L Silverstein
Cornell University · USCleveland Clinic · USCleveland State University · USRockefeller University · US

Funding

SCOR IN MOLECULAR MEDICINE AND ATHEROSCLEROSISP50HL056987 · NHLBI · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI FISHMAN, DONALD A · 1997 to 2001
$2.4M
MYELOPEROXIDASE, OXIDANT STRESS AND ATHEROGENESISR01HL062526 · NHLBI · CLEVELAND CLINIC LERNER COL/MED-CWRU · PI HAZEN, STANLEY L · 1999 to 2004
$1.4M
MOLECULAR AND CELL BIOLOGY OF CD36 A TSP RECEPTORR01HL042540 · NHLBI · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI SILVERSTEIN, ROY L · 1989 to 2000
$288k
NHLBI NIH HHS HL-42540NHLBI NIH HHS HL-56987NHLBI NIH HHS HL-62526
6 · The paper itself

Abstract

Macrophage scavenger receptors have been implicated as key players in the pathogenesis of atherosclerosis. To assess the role of the class B scavenger receptor CD36 in atherogenesis, we crossed a CD36-null strain with the atherogenic apo E-null strain and quantified lesion development. There was a 76.5% decrease in aortic tree lesion area (Western diet) and a 45% decrease in aortic sinus lesion area (normal chow) in the CD36-apo E double-null mice when compared with controls, despite alterations in lipoprotein profiles that often correlate with increased atherogenicity. Macrophages derived from CD36-apo E double-null mice bound and internalized more than 60% less copper-oxidized LDL and LDL modified by monocyte-generated reactive nitrogen species. A similar inhibition of in vitro lipid accumulation and foam cell formation after exposure to these ligands was seen. These results support a major role for CD36 in atherosclerotic lesion development in vivo and suggest that blockade of CD36 can be protective even in more extreme proatherogenic circumstances.

Indexed as

AnimalsApolipoproteins EArteriosclerosisCD36 AntigensCells, CulturedCholesterolFemaleLipoproteins, LDLMacrophages, PeritonealMaleMiceMice, Inbred C57BLReceptors, ImmunologicReceptors, ScavengerTriglyceridesWeight GainApolipoproteins ECD36 AntigensCholesterolLipoproteins, LDLoxidized low density lipoproteinReceptors, ImmunologicReceptors, ScavengerTriglycerides

Identifiers

PMID10772649
PMCPMC300837
OpenAlexW2153245546

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.