ArticleJournal of lipid research2015
Apolipoprotein A-I mimetic peptide 4F blocks sphingomyelinase-induced LDL aggregation.
Article in Journal of lipid research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- High cholesterol absorption efficiency enhances proatherogenic properties of low-density lipoprotein particles.Journal of internal medicine · 2026Article
- Bioactive peptides targeting dyslipidemia and atherosclerosis: from computational discovery and data bottlenecks to precision medicine translation.Frontiers in molecular biosciences · 2026Review
- Beyond cholesterol: linking the conformation of apolipoprotein B to atherogenesis.Current opinion in lipidology · 2025Review
- Mechanisms modulating foam cell formation in the arterial intima: exploring new therapeutic opportunities in atherosclerosis.Frontiers in cardiovascular medicine · 2024Review
- Apolipoproteins as potential communicators play an essential role in the pathogenesis and treatment of early atherosclerosis.International journal of biological sciences · 2023Review
- Modified Lipoproteins Induce Arterial Wall Inflammation During Atherogenesis.Frontiers in cardiovascular medicine · 2022Review
- Oxidized phospholipids cause changes in jejunum mucus that induce dysbiosis and systemic inflammation.Journal of lipid research · 2022Article
- Apolipoprotein and LRP1-Based Peptides as New Therapeutic Tools in Atherosclerosis.Journal of clinical medicine · 2021Review
- Current Understanding of the Immunomodulatory Activities of High-Density Lipoproteins.Biomedicines · 2021Review
- Aggregation Susceptibility of Low-Density Lipoproteins-A Novel Modifiable Biomarker of Cardiovascular Risk.Journal of clinical medicine · 2021Review
- Subcutaneous Administration of Apolipoprotein J-Derived Mimetic Peptide d-[113-122]apoJ Improves LDL and HDL Function and Prevents Atherosclerosis in LDLR-KO Mice.Biomolecules · 2020Article
- The Apolipoprotein A-I Mimetic L-4F Attenuates Monocyte Activation and Adverse Cardiac Remodeling after Myocardial Infarction.International journal of molecular sciences · 2020Article
- High-density Lipoprotein and Low-density Lipoprotein Therapeutic Approaches in Acute Coronary Syndromes.Current cardiology reviews · 2017Review
- High-density lipoprotein mimetics: promises and challenges.The Biochemical journal · 2015Review
- Lipid-laden foam cells in the pathology of atherosclerosis: shedding light on new therapeutic targets.Expert opinion on therapeutic targetsReview
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 3 countries.
Funding
Abstract
Lipolytic modification of LDL particles by SMase generates LDL aggregates with a strong affinity for human arterial proteoglycans and may so enhance LDL retention in the arterial wall. Here, we evaluated the effects of apoA-I mimetic peptide 4F on structural and functional properties of the SMase-modified LDL particles. LDL particles with and without 4F were incubated with SMase, after which their aggregation, structure, and proteoglycan binding were analyzed. At a molar ratio of L-4F to apoB-100 of 2.5 to 20:1, 4F dose-dependently inhibited SMase-induced LDL aggregation. At a molar ratio of 20:1, SMase-induced aggregation was fully blocked. Binding of 4F to LDL particles inhibited SMase-induced hydrolysis of LDL by 10% and prevented SMase-induced LDL aggregation. In addition, the binding of the SMase-modified LDL particles to human aortic proteoglycans was dose-dependently inhibited by pretreating LDL with 4F. The 4F stabilized apoB-100 conformation and inhibited SMase-induced conformational changes of apoB-100. Molecular dynamic simulations showed that upon binding to protein-free LDL surface, 4F locally alters membrane order and fluidity and induces structural changes to the lipid layer. Collectively, 4F stabilizes LDL particles by preventing the SMase-induced conformational changes in apoB-100 and so blocks SMase-induced LDL aggregation and the resulting increase in LDL retention.
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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.