Evidence map›Paper›PMID 24903227›Full record

ReviewExperimental & molecular medicine2014

CD36, a scavenger receptor implicated in atherosclerosis.

Young Mi Park

Open access · goldAbstract readReview
In one paragraph

Review in Experimental & molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 260 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
260citing papers in PubMed, 4 pooled it
14.4field-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

260 citing papers in PubMed, 4 syntheses or guidelines pooled it, 500 citations in OpenAlex.

  1. Pooled it
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  5. Article
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  7. Review
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  12. Circulating Liver-Derived and CD36Journal of extracellular vesicles · 2026
    Article
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  14. Review
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200 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Young Mi Park1] Department of Molecular Medicine, Ewha Womans University School of Medicine, Seoul, Republic of Korea [2] Ewha Global Top 5 Research Program, Ewha Womans University, Seoul, Republic of Korea.
Ewha Womans University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD36 is a membrane glycoprotein that is present on various types of cells, including monocytes, macrophages, microvascular endothelial cells, adipocytes and platelets. Macrophage CD36 participates in atherosclerotic arterial lesion formation through its interaction with oxidized low-density lipoprotein (oxLDL), which triggers signaling cascades for inflammatory responses. CD36 functions in oxLDL uptake and foam cell formation, which is the initial critical stage of atherosclerosis. In addition, oxLDL via CD36 inhibits macrophage migration, which may be a macrophage-trapping mechanism in atherosclerotic lesions. The role of CD36 was examined in in vitro studies and in vivo experiments, which investigated various functions of CD36 in atherosclerosis and revealed that CD36 deficiency reduces atherosclerotic lesion formation. Platelet CD36 also promotes atherosclerotic inflammatory processes and is involved in thrombus formation after atherosclerotic plaque rupture. Because CD36 is an essential component of atherosclerosis, defining the function of CD36 and its corresponding signaling pathway may lead to a new treatment strategy for atherosclerosis.

Indexed as

AnimalsAtherosclerosisCD36 AntigensHumansMacrophagesPlaque, AtheroscleroticCD36 Antigens

Identifiers

PMID24903227
PMCPMC4081553
OpenAlexW2064760068

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.