ArticleScientific reports2017
Cigarette smoke extract profoundly suppresses TNFα-mediated proinflammatory gene expression through upregulation of ATF3 in human coronary artery endothelial cells.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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
28 citing papers in PubMed, 37 citations in OpenAlex.
- Multiomic Reference Map of Endothelial Mechanosensitive Pathways Under Athero- and Erosion-Prone Flow.Journal of the American Heart Association · 2026Article
- Pathogenesis of plaque erosion.Trends in cardiovascular medicine · 2026Review
- Cellular and Molecular Mechanisms of Vascular Endothelial Injury Induced by Cigarette Smoke and Cigarette Smoke Extract in Atherosclerosis.Journal of inflammation research · 2026Review
- Biomarkers Differentiating Plaque Erosion from Stable Plaque.Current atherosclerosis reports · 2025Review
- Coronary Artery Disease Risk Variant Dampens the Expression of CALCRL by Reducing HSF Binding to Shear Stress Responsive Enhancer in Endothelial Cells In Vitro.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Interleukin-1β polarization in M1 macrophage mediates myocardial fibrosis in diabetes.International immunopharmacology · 2024Article
- Alpha-1 antitrypsin inhibits fractalkine-mediated monocyte-lung endothelial cell interactions.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Quantitative proteomic analyses uncover regulatory roles of Nrf2 in human endothelial cells.Cell stress & chaperones · 2023Article
- Early aging and premature vascular aging in chronic kidney disease.Clinical kidney journal · 2023Review
- A Nrf2-OSGIN1&2-HSP70 axis mediates cigarette smoke-induced endothelial detachment: implications for plaque erosion.Cardiovascular research · 2023Article
- The Role of Smoking in the Mechanisms of Development of Chronic Obstructive Pulmonary Disease and Atherosclerosis.International journal of molecular sciences · 2023Review
- ATF3 in atherosclerosis: a controversial transcription factor.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Epigenetic Regulation ofCirculation research · 2022Article
- Toll-Like Receptors/TNF-BioMed research international · 2022Article
- Cigarette smoke exposure attenuates the induction of antigen-specific IgA in the murine upper respiratory tract.Mucosal immunology · 2021Article
- Identification of the haemodynamic environment permissive for plaque erosion.Scientific reports · 2021Article
- IL-36 Cytokines Promote Inflammation in the Lungs of Long-Term Smokers.American journal of respiratory cell and molecular biology · 2021Article
- Small, Dense Low-Density Lipoprotein-Cholesterol and Atherosclerosis: Relationship and Therapeutic Strategies.Frontiers in cardiovascular medicine · 2021Review
- Prediction of Mechanosensitive Genes in Vascular Endothelial Cells Under High Wall Shear Stress.Frontiers in genetics · 2021Article
- Lung-derived HMGB1 is detrimental for vascular remodeling of metabolically imbalanced arterial macrophages.Nature communications · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Endothelial dysfunction caused by the combined action of disturbed flow, inflammatory mediators and oxidants derived from cigarette smoke is known to promote coronary atherosclerosis and increase the likelihood of myocardial infarctions and strokes. Conversely, laminar flow protects against endothelial dysfunction, at least in the initial phases of atherogenesis. We studied the effects of TNFα and cigarette smoke extract on human coronary artery endothelial cells under oscillatory, normal laminar and elevated laminar shear stress for a period of 72 hours. We found, firstly, that laminar flow fails to overcome the inflammatory effects of TNFα under these conditions but that cigarette smoke induces an anti-oxidant response that appears to reduce endothelial inflammation. Elevated laminar flow, TNFα and cigarette smoke extract synergise to induce expression of the transcriptional regulator activating transcription factor 3 (ATF3), which we show by adenovirus driven overexpression, decreases inflammatory gene expression independently of activation of nuclear factor-κB. Our results illustrate the importance of studying endothelial dysfunction in vitro over prolonged periods. They also identify ATF3 as an important protective factor against endothelial dysfunction. Modulation of ATF3 expression may represent a novel approach to modulate proinflammatory gene expression and open new therapeutic avenues to treat proinflammatory diseases.
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.