ArticleInternational journal of molecular sciences2020
Signaling Pathways Potentially Responsible for Foam Cell Formation: Cholesterol Accumulation or Inflammatory Response-What is First?
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
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Who cites it
30 citing papers in PubMed, 41 citations in OpenAlex.
- Hexosamine Biosynthetic Pathway and Fatty Acid β-Oxidative Imbalance: A Key Mechanism by Which Abnormal Macrophage Lipophagy Promotes Atherosclerosis in Diabetes.Cardiovascular drugs and therapy · 2026Review
- New Advances in the Mechanisms and Therapeutic Strategies of Gut Microbiota in Regulating Glycolipid Metabolism to Combat Atherosclerosis.Journal of cardiovascular translational research · 2026Review
- Mouse Model of Low-density Lipoprotein Desialylation In Vivo.Current medicinal chemistry · 2026Article
- The IRE1α Pathway Links Endoplasmic Reticulum Stress to Atherosclerosis-Related Inflammation and Lipid Accumulation.Mediators of inflammation · 2026Article
- Rhynchophylline alleviates early atherosclerosis by attenuating oxidized low-density lipoprotein-induced foam cell formation and endothelial dysfunction.Molecular and cellular biochemistry · 2026Article
- Ultrasound-driven atherosclerosis nanomedicine: from mechanical, cavitation, and sonodynamic therapies to bedside translation.Journal of nanobiotechnology · 2025Review
- Directly Measuring Atherogenic Lipoprotein Kinetics in Zebrafish With the Photoconvertible LipoTimer Reporter.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Targeting fatty acid synthase reduces aortic atherosclerosis and inflammation.Communications biology · 2025Article
- The role of the ER stress sensor IRE1 in cardiovascular diseases.Molecular and cellular biochemistry · 2025Review
- Evidence for the Involvement of Gene Regulation of Inflammatory Molecules in the Accumulation of Intracellular Cholesterol: The Mechanism of Foam Cell Formation in Atherosclerosis.Current medicinal chemistry · 2025Article
- Protective effect of SERCA2a-SUMOylation by SUMO-1 on diabetes-induced atherosclerosis and aortic vascular injury.Molecular and cellular biochemistry · 2025Article
- We Must Abandon the Myth: Oxidized Low-density Lipoprotein is not a Lipoprotein that Plays a Key Role in Atherogenesis.Current medicinal chemistry · 2025Review
- Mitochondrial DNA Mutations as a Factor in the Heritability of Atherosclerosis and Other Diseases.Current medicinal chemistry · 2025Review
- The Link between Lipids and Inflammation: Focus on Targeting Sialidase Activity as a Novel Strategy for Anti-Atherosclerotic Therapy.Current medicinal chemistry · 2025Article
- Ginsenoside RbChinese herbal medicines · 2024Review
- Single-particle rotational microrheology enables pathological staging of macrophage foaming and antiatherosclerotic studies.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Applied physiology: gut microbiota and antimicrobial therapy.European journal of applied physiology · 2024Review
- Non-oxidativeCurrent medicinal chemistry · 2024Article
- Review
- CD36/Lyn kinase interactions within macrophages promotes pulmonary fibrosis in response to oxidized phospholipid.Respiratory research · 2023Article
Corrections and comments
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Authors and funding
16 authors at 12 institutions in 4 countries.
Funding
Abstract
Accumulation of lipid-laden (foam) cells in the arterial wall is known to be the earliest step in the pathogenesis of atherosclerosis. There is almost no doubt that atherogenic modified low-density lipoproteins (LDL) are the main sources of accumulating lipids in foam cells. Atherogenic modified LDL are taken up by arterial cells, such as macrophages, pericytes, and smooth muscle cells in an unregulated manner bypassing the LDL receptor. The present study was conducted to reveal possible common mechanisms in the interaction of macrophages with associates of modified LDL and non-lipid latex particles of a similar size. To determine regulatory pathways that are potentially responsible for cholesterol accumulation in human macrophages after the exposure to naturally occurring atherogenic or artificially modified LDL, we used transcriptome analysis. Previous studies of our group demonstrated that any type of LDL modification facilitates the self-association of lipoprotein particles. The size of such self-associates hinders their interaction with a specific LDL receptor. As a result, self-associates are taken up by nonspecific phagocytosis bypassing the LDL receptor. That is why we used latex beads as a stimulator of macrophage phagocytotic activity. We revealed at least 12 signaling pathways that were regulated by the interaction of macrophages with the multiple-modified atherogenic naturally occurring LDL and with latex beads in a similar manner. Therefore, modified LDL was shown to stimulate phagocytosis through the upregulation of certain genes. We have identified at least three genes (
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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 Socratic graph.