Evidence map›Paper›PMID 38790688›Full record

ReviewAntioxidants (Basel, Switzerland)2024

Radical Oxygen Species, Oxidized Low-Density Lipoproteins, and Lectin-like Oxidized Low-Density Lipoprotein Receptor 1: A Vicious Circle in Atherosclerotic Process.

Marco Munno, Alice Mallia, Arianna Greco, Gloria Modafferi, Cristina Banfi, Sonia Eligini

Abstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

35 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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  5. [Active Oxygen Influences Foam Macrophage Formation by Regulating Peroxisome Proliferator-Activated Receptor-γ Expression].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026
    Article
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  13. Novel insights of ferroptosis in atherosclerosis progression.Frontiers in cell and developmental biology · 2026
    Review
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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

6 authors.

Marco MunnoUnit of Functional Proteomics, Metabolomics and Network Analysis, Centro Cardiologico Monzino, 20138 Milan, Italy.ORCID 0009-0008-6033-7891
Alice MalliaUnit of Functional Proteomics, Metabolomics and Network Analysis, Centro Cardiologico Monzino, 20138 Milan, Italy.ORCID 0000-0002-7088-9074
Arianna GrecoUnit of Functional Proteomics, Metabolomics and Network Analysis, Centro Cardiologico Monzino, 20138 Milan, Italy.
Gloria ModafferiUnit of Functional Proteomics, Metabolomics and Network Analysis, Centro Cardiologico Monzino, 20138 Milan, Italy.
Cristina BanfiUnit of Functional Proteomics, Metabolomics and Network Analysis, Centro Cardiologico Monzino, 20138 Milan, Italy.ORCID 0000-0003-3346-9879
Sonia EliginiUnit of Functional Proteomics, Metabolomics and Network Analysis, Centro Cardiologico Monzino, 20138 Milan, Italy.ORCID 0000-0002-5507-6737

Funding

Italian Ministry of Health, Rome, Italy Ricerca corrente
6 · The paper itself

Abstract

Atherosclerosis is a complex condition that involves the accumulation of lipids and subsequent plaque formation in the arterial intima. There are various stimuli, cellular receptors, and pathways involved in this process, but oxidative modifications of low-density lipoprotein (ox-LDL) are particularly important in the onset and progression of atherosclerosis. Ox-LDLs promote foam-cell formation, activate proinflammatory pathways, and induce smooth-muscle-cell migration, apoptosis, and cell death. One of the major receptors for ox-LDL is LOX-1, which is upregulated in several cardiovascular diseases, including atherosclerosis. LOX-1 activation in endothelial cells promotes endothelial dysfunction and induces pro-atherogenic signaling, leading to plaque formation. The binding of ox-LDLs to LOX-1 increases the generation of reactive oxygen species (ROS), which can induce LOX-1 expression and oxidize LDLs, contributing to ox-LDL generation and further upregulating LOX-1 expression. This creates a vicious circle that is amplified in pathological conditions characterized by high plasma levels of LDLs. Although LOX-1 has harmful effects, the clinical significance of inhibiting this protein remains unclear. Further studies both in vitro and in vivo are needed to determine whether LOX-1 inhibition could be a potential therapeutic target to counteract the atherosclerotic process.

Indexed as

atherosclerosisLOX-1ox-LDLradical oxygen species

Identifiers

PMID38790688
PMCPMC11118168

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.