ArticleNature metabolism2019
Endothelial TGF-β signalling drives vascular inflammation and atherosclerosis.
Article in Nature metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 215 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
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
215 citing papers in PubMed, 330 citations in OpenAlex.
- Review
- Integrative Single-Cell Transcriptomics, Multi-Omics Analyses, and Computational Pharmacology Reveal Macrophage Heterogeneity and the Putative THBS1-CD36 Axis in Coronary Atherosclerosis.Chemical biology & drug design · 2026Article
- Smooth Muscle Cell Plasticity as a Central Determinant of Plaque Stability.Current atherosclerosis reports · 2026Review
- SNAI2/SLUG: a key regulator of endothelial-to-mesenchymal transition and vascular remodeling in cardiovascular diseases.Journal of cardiothoracic surgery · 2026Review
- Mechanism of Shuangshen Xionglian Granule in Attenuating EndMT in Atherosclerosis via the FGFR1-TGF-β/Smad2 Axis.Molecular nutrition & food research · 2026Article
- Metabolic control of smooth muscle cell phenotype switching in atherosclerosis.Science advances · 2026Article
- USP5 Stabilizes TGFBR1 to Drive Vascular Smooth Muscle Cell Senescence and Atherosclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Endothelial cells modulate immune cell responses during atherosclerosis.Trends in immunology · 2026Review
- Pan-Peroxisome Proliferator-Activated Receptor Agonist IVA337 Alleviates Secondary Lymphedema via Inhibiting TGFβ/SMAD2/3 Signaling Pathway.bioRxiv : the preprint server for biology · 2026Article
- Multiomic Reference Map of Endothelial Mechanosensitive Pathways Under Athero- and Erosion-Prone Flow.Journal of the American Heart Association · 2026Article
- Gut Microbiota and Atherosclerotic Plaque Instability: Cellular and Molecular Mechanisms.International journal of molecular sciences · 2026Review
- Cell-Type-Specific Regulation of Ferroptosis in Atherosclerosis: Mechanisms and Therapeutic Potential of Natural Products.Cell biochemistry and function · 2026Review
- SGLT2 Inhibitors Attenuate Neutrophil-Mediated Endothelial Injury in Coronary Artery Disease With Type 2 Diabetes Mellitus Through a GREM1-Associated Smad Signaling Axis.Journal of cardiovascular pharmacology · 2026Article
- Review
- The exploration to identify key molecules in the interaction between endothelial cells and mono-macrophages in atherosclerosis based on the single cell transcriptome.BMC cardiovascular disorders · 2026Article
- Circular RNA-mediated regulation of key signaling pathways in cardiovascular diseases: a review.Journal of advanced research · 2026Review
- Intervening at the microbial crossroads: targeting inflammation across the oral-gut-reproductive microbiome crosstalk in atherosclerosis.Antonie van Leeuwenhoek · 2026Review
- TGF-β and TNF-α Signaling Crosstalk in Human Coronary Artery Cells.International journal of molecular sciences · 2026Article
- Lipid-based nanosystems for atherosclerosis treatment: Evolving approaches and novel therapeutic strategies.Acta pharmaceutica Sinica. B · 2026Review
- SPP1BMC medicine · 2026Article
155 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
27 authors at 10 institutions in 4 countries.
Funding
Abstract
Atherosclerosis is a progressive vascular disease triggered by interplay between abnormal shear stress and endothelial lipid retention. A combination of these and, potentially, other factors leads to a chronic inflammatory response in the vessel wall, which is thought to be responsible for disease progression characterized by a buildup of atherosclerotic plaques. Yet molecular events responsible for maintenance of plaque inflammation and plaque growth have not been fully defined. Here we show that endothelial TGFβ signaling is one of the primary drivers of atherosclerosis-associated vascular inflammation. Inhibition of endothelial TGFβ signaling in hyperlipidemic mice reduces vessel wall inflammation and vascular permeability and leads to arrest of disease progression and regression of established lesions. These pro-inflammatory effects of endothelial TGFβ signaling are in stark contrast with its effects in other cell types and identify it as an important driver of atherosclerotic plaque growth and show the potential of cell-type specific therapeutic intervention aimed at control of this disease.
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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.