ArticlePLoS genetics2014
Plasma cholesterol-induced lesion networks activated before regression of early, mature, and advanced atherosclerosis.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 68 citations in OpenAlex.
- Allele-specific control of rodent and human lncRNA KMT2E-AS1 promotes hypoxic endothelial pathology in pulmonary hypertension.Science translational medicine · 2024Pooled it
- Systematic Overview of Solid Particles and Their Host Responses.Frontiers in immunology · 2018Pooled it
- Gene regulatory network analysis identifies auranofin as an anti-atherosclerotic drug.Nature communications · 2026Article
- Vascular cognitive impairment and dementia: Prevention, treatments, mechanisms and management options for the future.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- Remnant cholesterol is associated with unstable carotid plaque in a neurologically healthy population.Stroke and vascular neurology · 2025Article
- White Tea Reduces Dyslipidemia, Inflammation, and Oxidative Stress in the Aortic Arch in a Model of Atherosclerosis Induced by Atherogenic Diet in ApoE Knockout Mice.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Developing Theoretical Models for Atherosclerotic Lesions: A Methodological Approach Using Interdisciplinary Insights.Life (Basel, Switzerland) · 2024Article
- Single-Cell Gene-Regulatory Networks of Advanced Symptomatic Atherosclerosis.Circulation research · 2024Article
- Cholesterol lowering depletes atherosclerotic lesions of smooth muscle cell-derived fibromyocytes and chondromyocytes.Nature cardiovascular research · 2024Article
- Metabolic and Vascular Risk Factor Variability Over 25 Years Relates to Midlife Brain Volume and Cognition.Journal of Alzheimer's disease : JAD · 2023Article
- Peptidomimetics for CVD screened via TRADD-TRAF2 complex interface assessments.In silico pharmacology · 2023Article
- A Unified Model of Age-Related Cardiovascular Disease.Biology · 2022Review
- Prevention of atherosclerosis from childhood.Nature reviews. Cardiology · 2022Review
- Splicing machinery is impaired in rheumatoid arthritis, associated with disease activity and modulated by anti-TNF therapy.Annals of the rheumatic diseases · 2022Article
- Connections for Matters of the Heart: Network Medicine in Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2022Review
- SRSF10: an atypical splicing regulator with critical roles in stress response, organ development, and viral replication.RNA (New York, N.Y.) · 2021Review
- Higher visit-to-visit total cholesterol variability is associated with lower cognitive function among middle-aged and elderly Chinese men.Scientific reports · 2020Article
- Can atherosclerosis be cured?Current opinion in lipidology · 2019Review
- Contribution of Gene Regulatory Networks to Heritability of Coronary Artery Disease.Journal of the American College of Cardiology · 2019Article
- Variability in Total Cholesterol Concentration Is Associated With the Risk of Dementia: A Nationwide Population-Based Cohort Study.Frontiers in neurology · 2019Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 5 countries.
Funding
Abstract
Plasma cholesterol lowering (PCL) slows and sometimes prevents progression of atherosclerosis and may even lead to regression. Little is known about how molecular processes in the atherosclerotic arterial wall respond to PCL and modify responses to atherosclerosis regression. We studied atherosclerosis regression and global gene expression responses to PCL (≥80%) and to atherosclerosis regression itself in early, mature, and advanced lesions. In atherosclerotic aortic wall from Ldlr(-/-)Apob (100/100) Mttp (flox/flox)Mx1-Cre mice, atherosclerosis regressed after PCL regardless of lesion stage. However, near-complete regression was observed only in mice with early lesions; mice with mature and advanced lesions were left with regression-resistant, relatively unstable plaque remnants. Atherosclerosis genes responding to PCL before regression, unlike those responding to the regression itself, were enriched in inherited risk for coronary artery disease and myocardial infarction, indicating causality. Inference of transcription factor (TF) regulatory networks of these PCL-responsive gene sets revealed largely different networks in early, mature, and advanced lesions. In early lesions, PPARG was identified as a specific master regulator of the PCL-responsive atherosclerosis TF-regulatory network, whereas in mature and advanced lesions, the specific master regulators were MLL5 and SRSF10/XRN2, respectively. In a THP-1 foam cell model of atherosclerosis regression, siRNA targeting of these master regulators activated the time-point-specific TF-regulatory networks and altered the accumulation of cholesterol esters. We conclude that PCL leads to complete atherosclerosis regression only in mice with early lesions. Identified master regulators and related PCL-responsive TF-regulatory networks will be interesting targets to enhance PCL-mediated regression of mature and advanced atherosclerotic lesions.
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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.