ArticleEuropean heart journal2018
Susceptibility of low-density lipoprotein particles to aggregate depends on particle lipidome, is modifiable, and associates with future cardiovascular deaths.
Article in European heart journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04152291 (The Effect of Ethyl Eicosapentaenoic Acid on Circulating Low-density Lipoproteins and Plasma Lipid Metabolism in Healthy Volunteers), which is not on this map. Cited by 94 papers.
What it found
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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.
The Effect of Ethyl Eicosapentaenoic Acid on Circulating Low-density Lipoproteins and Plasma Lipid Metabolism in Healthy Volunteers
Who cites it
94 citing papers in PubMed, 181 citations in OpenAlex.
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- Increased transvascular retention of atherogenic lipoproteins in type 2 diabetes relates to their enhanced proteoglycan binding.JCI insight · 2026Article
- Circulating ceramides and sphingomyelins: key biomarkers and targets in cardiovascular prevention.Science China. Life sciences · 2026Review
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- Effect of HDL disk and LDL dimer presence on lipoprotein particle number determination and subclassification.Analytical and bioanalytical chemistry · 2026Article
- Risk Haplotype of BTNL2 Predisposes Male Patients to NSTEMI: A Genetic and Functional Study.Research square · 2026Article
- Ceramide as a key regulatory factor in the impact of dietary inflammatory index on plaque stability.Scientific reports · 2026Article
- Sphingolipid Metabolism: A Pathological Hub Linking Lipid Dysregulation and Chronic Inflammation in Atherosclerotic Cardiovascular Disease.Journal of inflammation research · 2026Review
- Lipidomic Signature of Patients with Familial Hypercholesterolemia Carrying Pathogenic Variants Unveils a Cue of Increased Cardiovascular Risk.International journal of molecular sciences · 2025Article
- Icosapent ethyl-induced lipoprotein remodeling and its impact on cardiovascular disease risk markers in normolipidemic individuals.JCI insight · 2025Article
- Beyond cholesterol: linking the conformation of apolipoprotein B to atherogenesis.Current opinion in lipidology · 2025Review
- Ceramides in cardiovascular disease: emerging role as independent risk predictors and novel therapeutic targets.Cardiovascular research · 2025Review
- Burden of ischemic stroke attributable to high low-density lipoprotein cholesterol in China from the global burden of disease study 2021.Scientific reports · 2025Article
- Sex-specific lipidomic signatures in aortic valve disease reflect differential fibro-calcific progression.Nature communications · 2025Article
- Apolipoprotein B-containing lipoproteins in atherogenesis.Nature reviews. Cardiology · 2025Review
- Reduced blood EPAC1 protein levels as a marker of severe coronary artery disease: the role of hypoxic foam cell-transformed smooth muscle cells.Journal of translational medicine · 2025Article
- Modern therapy of patients with lupus erythematosus must include appropriate management of their heightened rates of atherosclerotic cardiovascular events: a literature update.Lupus science & medicine · 2025Review
34 more citing papers are in PubMed but not listed here.
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Authors and funding
32 authors at 13 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aims: Low-density lipoprotein (LDL) particles cause atherosclerotic cardiovascular disease (ASCVD) through their retention, modification, and accumulation within the arterial intima. High plasma concentrations of LDL drive this disease, but LDL quality may also contribute. Here, we focused on the intrinsic propensity of LDL to aggregate upon modification. We examined whether inter-individual differences in this quality are linked with LDL lipid composition and coronary artery disease (CAD) death, and basic mechanisms for plaque growth and destabilization. Methods and results: We developed a novel, reproducible method to assess the susceptibility of LDL particles to aggregate during lipolysis induced ex vivo by human recombinant secretory sphingomyelinase. Among patients with an established CAD, we found that the presence of aggregation-prone LDL was predictive of future cardiovascular deaths, independently of conventional risk factors. Aggregation-prone LDL contained more sphingolipids and less phosphatidylcholines than did aggregation-resistant LDL. Three interventions in animal models to rationally alter LDL composition lowered its susceptibility to aggregate and slowed atherosclerosis. Similar compositional changes induced in humans by PCSK9 inhibition or healthy diet also lowered LDL aggregation susceptibility. Aggregated LDL in vitro activated macrophages and T cells, two key cell types involved in plaque progression and rupture. Conclusion: Our results identify the susceptibility of LDL to aggregate as a novel measurable and modifiable factor in the progression of human ASCVD.
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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.