ArticleJournal of cell science2007
Cholesterol suppresses cellular TGF-beta responsiveness: implications in atherogenesis.
Article in Journal of cell science, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis 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
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- Association between transforming growth factor-beta 1 T869C polymorphism and ischemic stroke: a meta-analysis.PloS one · 2013Pooled it
- Molecular Engineering of the Helminth TGF-β Mimetics, TGM1 and TGM4, Reveals a Novel Antagonist of TGF-β Signaling in Fibroblasts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- HDL Regulates TGFβ-Receptor Lipid Raft Partitioning, Restoring Contractile Features of Cholesterol-Loaded Vascular Smooth Muscle Cells.JACC. Basic to translational science · 2026Article
- Gender-specific association between a lipid composite index and asthma among US adults: insights from a population-based study.Lipids in health and disease · 2024Article
- TGF-β1 and TGFβR2 Gene Polymorphisms in Patients with Unstable Angina.Biomedicines · 2023Article
- Endocytosis of Peptidase Inhibitor SerpinE2 promotes Myocardial Fibrosis through activating ERK1/2 and β-catenin Signaling Pathways.International journal of biological sciences · 2022Article
- A multiphase model of growth factor-regulated atherosclerotic cap formation.Journal of mathematical biology · 2020Article
- Asthma and Obesity in Children.Biomedicines · 2020Review
- Lipid mechanisms in hallmarks of cancer.Molecular omics · 2020Review
- Toward a Membrane-Centric Biology.Frontiers in immunology · 2020Article
- Roles of Myosin-Mediated Membrane Trafficking in TGF-β Signaling.International journal of molecular sciences · 2019Review
- Prediction of putative small molecules for manipulation of enriched signalling pathways in hESC-derived early cardiovascular progenitors by bioinformatics analysis.IET systems biology · 2019Article
- CtBP promotes metastasis of breast cancer through repressing cholesterol and activating TGF-β signaling.Oncogene · 2019Article
- Pentabromopseudilin: a myosin V inhibitor suppresses TGF-β activity by recruiting the type II TGF-β receptor to lysosomal degradation.Journal of enzyme inhibition and medicinal chemistry · 2018Article
- Less cholesterol means better tumor killing for cytotoxic T9 cells.The Journal of experimental medicine · 2018Article
- Apolipoprotein E Promotes Invasion in Oral Squamous Cell Carcinoma.The American journal of pathology · 2017Article
- 7-Dehydrocholesterol (7-DHC), But Not Cholesterol, Causes Suppression of Canonical TGF-β Signaling and Is Likely Involved in the Development of Atherosclerotic Cardiovascular Disease (ASCVD).Journal of cellular biochemistry · 2017Article
- The TGF-β Family inCold Spring Harbor perspectives in biology · 2017Review
- Pentabromophenol suppresses TGF-β signaling by accelerating degradation of type II TGF-β receptors via caveolae-mediated endocytosis.Scientific reports · 2017Article
- DMSO Enhances TGF-β Activity by Recruiting the Type II TGF-β Receptor From Intracellular Vesicles to the Plasma Membrane.Journal of cellular biochemistry · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Hypercholesterolemia is a major causative factor for atherosclerotic cardiovascular disease. The molecular mechanisms by which cholesterol initiates and facilitates the process of atherosclerosis are not well understood. Here, we demonstrate that cholesterol treatment suppresses or attenuates TGF-beta responsiveness in all cell types studied as determined by measuring TGF-beta-induced Smad2 phosphorylation and nuclear translocation, TGF-beta-induced PAI-1 expression, TGF-beta-induced luciferase reporter gene expression and TGF-beta-induced growth inhibition. Cholesterol, alone or complexed in lipoproteins (LDL, VLDL), suppresses TGF-beta responsiveness by increasing lipid raft and/or caveolae accumulation of TGF-beta receptors and facilitating rapid degradation of TGF-beta and thus suppressing TGF-beta-induced signaling. Conversely, cholesterol-lowering agents (fluvastatin and lovastatin) and cholesterol-depleting agents (beta-cyclodextrin and nystatin) enhance TGF-beta responsiveness by increasing non-lipid raft microdomain accumulation of TGF-beta receptors and facilitating TGF-beta-induced signaling. Furthermore, the effects of cholesterol on the cultured cells are also found in the aortic endothelium of ApoE-null mice fed a high-cholesterol diet. These results suggest that high cholesterol contributes to atherogenesis, at least in part, by suppressing TGF-beta responsiveness in vascular cells.
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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.