ArticleThe Journal of clinical investigation2005
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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 32 papers.
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.
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.
Who cites it
32 citing papers in PubMed.
- An Update of Oxidative Stress in Atherosclerosis with Emphasis on the LOX-1-NLRP3 Inflammasome Axis.Current atherosclerosis reports · 2026Review
- Graphene Nanoplatelets Suppress Foam Cell Formation and Atherogenic Inflammation in Macrophages.Cellular and molecular bioengineering · 2026Article
- Histone demethylase LSD1 regulates lipid homeostasis duringiScience · 2025Article
- Modified Lipoproteins Induce Arterial Wall Inflammation During Atherogenesis.Frontiers in cardiovascular medicine · 2022Review
- Aggregation Susceptibility of Low-Density Lipoproteins-A Novel Modifiable Biomarker of Cardiovascular Risk.Journal of clinical medicine · 2021Review
- Vimentin deficiency in macrophages induces increased oxidative stress and vascular inflammation but attenuates atherosclerosis in mice.Scientific reports · 2018Article
- Article
- Applications and Limitations of Mouse Models for Understanding Human Atherosclerosis.Cell metabolism · 2017Review
- Lanatoside C Promotes Foam Cell Formation and Atherosclerosis.Scientific reports · 2016Article
- CEP Is an Important and Ubiquitous Oxidation Specific Epitope Recognized by Innate Pattern Recognition Receptors.Circulation research · 2015Article
- Acidification of the intimal fluid: the perfect storm for atherogenesis.Journal of lipid research · 2015Review
- CD36-dependent 7-ketocholesterol accumulation in macrophages mediates progression of atherosclerosis in response to chronic air pollution exposure.Circulation research · 2014Article
- CD36, a scavenger receptor implicated in atherosclerosis.Experimental & molecular medicine · 2014Review
- The influence of innate and adaptive immune responses on atherosclerosis.Annual review of pathology · 2014Review
- Inflammatory therapeutic targets in coronary atherosclerosis-from molecular biology to clinical application.Frontiers in physiology · 2014Review
- Dietary carnosine prevents early atherosclerotic lesion formation in apolipoprotein E-null mice.Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- Oxidation-specific epitopes and immunological responses: Translational biotheranostic implications for atherosclerosis.Current opinion in pharmacology · 2013Review
- CD36, but not G2A, modulates efferocytosis, inflammation, and fibrosis following bleomycin-induced lung injury.Journal of lipid research · 2013Article
- The role of oxidized low-density lipoproteins in atherosclerosis: the myths and the facts.Mediators of inflammation · 2013Review
- Design and synthesis of a stable oxidized phospholipid mimic with specific binding recognition for macrophage scavenger receptors.Journal of medicinal chemistry · 2012Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophage scavenger receptors, such as CD36 and class A scavenger receptor (SR-A), have previously been thought to play a central role in foam cell formation and atherogenesis by mediating the uptake of oxidized LDL. In this issue of the JCI, Moore et al. report that Apoe mice deficient in either CD36 or SR-A did not have less atherosclerosis at the level of the aortic valve than did wild-type Apoe mice. In contrast, similar studies by previous investigators found that deletion of these receptors decreased atherogenesis. The reasons for the different results are not known, but these data suggest that the role of these receptors in atherogenesis remains unresolved.
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Registered trials
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.