ArticleScientific reports2018
Enzyme-modified non-oxidized LDL (ELDL) induces human coronary artery smooth muscle cell transformation to a migratory and osteoblast-like phenotype.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 22 papers, 1 of them a synthesis that pooled 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.
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
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Molecular Interactions Between Vascular Smooth Muscle Cells and Macrophages in Atherosclerosis.Frontiers in cardiovascular medicine · 2021Pooled it
- Desialylated vs. Oxidized LDL: Sialidase Inhibitors as Promising Antiatherosclerotic Agents.Current atherosclerosis reports · 2026Review
- The serum ANGPTL4 level and severe coronary artery calcification: from association to risk prediction using a nomogram.Frontiers in cardiovascular medicine · 2026Article
- Review
- The Link between Lipids and Inflammation: Focus on Targeting Sialidase Activity as a Novel Strategy for Anti-Atherosclerotic Therapy.Current medicinal chemistry · 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
- PAC1 deficiency reduces chondrogenesis in atherosclerotic lesions of hypercholesterolemic ApoE-deficient mice.BMC cardiovascular disorders · 2023Article
- Pro-Calcifying Role of Enzymatically Modified LDL (eLDL) in Aortic Valve Sclerosis via Induction of IL-6 and IL-33.Biomolecules · 2023Article
- Single-cell RNA sequencing reveals the vascular smooth muscle cell phenotypic landscape in aortic aneurysm.Cell communication and signaling : CCS · 2023Article
- Atherosclerosis Calcification: Focus on Lipoproteins.Metabolites · 2023Review
- How vascular smooth muscle cell phenotype switching contributes to vascular disease.Cell communication and signaling : CCS · 2022Review
- Rapamycin and Paclitaxel Affect Human Aortic Smooth Muscle Cells-Derived Foam Cells Viability and Proliferation.Brazilian journal of cardiovascular surgery · 2022Article
- Possible causes of atherosclerosis: lncRNAAnnals of translational medicine · 2022Article
- Insights Into the Role of Mitochondria in Vascular Calcification.Frontiers in cardiovascular medicine · 2022Review
- Macrophages in Atherosclerosis, First or Second Row Players?Biomedicines · 2021Review
- Role of Glycosylation in Vascular Calcification.International journal of molecular sciences · 2021Review
- Emulating Early Atherosclerosis in a Vascular Microphysiological System Using Branched Tissue-Engineered Blood Vessels.Advanced biology · 2021Article
- Lysosome (Dys)function in Atherosclerosis-A Big Weight on the Shoulders of a Small Organelle.Frontiers in cell and developmental biology · 2021Review
- Neutrophils as a Novel Target of Modified Low-Density Lipoproteins and an Accelerator of Cardiovascular Diseases.International journal of molecular sciences · 2020Review
- Role of Phagocytosis in the Pro-Inflammatory Response in LDL-Induced Foam Cell Formation; a Transcriptome Analysis.International journal of molecular sciences · 2020Article
Corrections and comments
- Expression of concern
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Enzyme modified non-oxidative LDL (ELDL) is effectively taken up by vascular smooth muscle cells (SMC) and mediates transition into foam cells and produces phenotypic changes in SMC function. Our data show that incubation of human coronary artery SMC (HCASMC) with low concentration of ELDL (10 μg/ml) results in significantly enhanced foam cell formation compared to oxidized LDL (200 μg/ml; p < 0.01) or native LDL (200 μg/ml; p < 0.01). Bioinformatic network analysis identified activation of p38 MAPK, NFkB, ERK as top canonical pathways relevant for biological processes linked to cell migration and osteoblastic differentiation in ELDL-treated cells. Functional studies confirmed increased migration of HCASMC upon stimulation with ELDL (10 μg/ml) or Angiopoietin like protein 4, (ANGPTL4, 5 μg/ml), and gain in osteoblastic gene profile with significant increase in mRNA levels for DMP-1, ALPL, RUNX2, OPN/SPP1, osterix/SP7, BMP and reduction in mRNA for MGP and ENPP1. Enhanced calcification of HCASMC by ELDL was demonstrated by Alizarin Red staining. In summary, ELDL is highly potent in inducing foam cells in HCASMC and mediates a phenotypic switch with enhanced migration and osteoblastic gene profile. These results point to the potential of ELDL to induce migratory and osteoblastic effects in human smooth muscle cells with potential implications for migration and calcification of SMCs in human atherosclerosis.
Indexed as
Identifiers
What OpenQuestion holds
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.