ArticleScientific reports2022
Uncovering emergent phenotypes in endothelial cells by clustering of surrogates of cardiovascular risk factors.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed, 19 citations in OpenAlex.
- The chemical composition of secondary organic aerosols regulates transcriptomic and metabolomic signaling in an epithelial-endothelial in vitro coculture.Particle and fibre toxicology · 2024Article
- Integrated systems biology approach identifies gene targets for endothelial dysfunction.Molecular systems biology · 2023Article
- MicroRNA-1 protects the endothelium in acute lung injury.JCI insight · 2023Article
- Additional improvement in regional myocardial ischemia after intracardiac injection of bone marrow cells during CABG surgery.Frontiers in cardiovascular medicine · 2023Article
- Diversity of arterial cell and phenotypic heterogeneity induced by high-fat and high-cholesterol diet.Frontiers in cell and developmental biology · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Endothelial dysfunction (ED) is a hallmark of atherosclerosis and is influenced by well-defined risk factors, including hypoxia, dyslipidemia, inflammation, and oscillatory flow. However, the individual and combined contributions to the molecular underpinnings of ED remain elusive. We used global gene expression in human coronary artery endothelial cells to identify gene pathways and cellular processes in response to chemical hypoxia, oxidized lipids, IL-1β induced inflammation, oscillatory flow, and these combined stimuli. We found that clustering of the surrogate risk factors differed from the sum of the individual insults that gave rise to emergent phenotypes such as cell proliferation. We validated these observations in samples of human coronary artery atherosclerotic plaques analyzed using single-cell RNA sequencing. Our findings suggest a hierarchical interaction between surrogates of CV risk factors and the advent of emergent phenotypes in response to combined stimulation in endothelial cells that may influence ED.
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Registered trials
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