ArticleScientific reports2022
Intermittent hypoxia inhibits epinephrine-induced transcriptional changes in human aortic endothelial cells.
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, 5 citations in OpenAlex.
- Elephant Seal Blubber Under Multiple Stressors: Persistent Organic Pollutants, Stress Hormones and Hydrostatic Pressure Alter Transcriptome, Lipolysis and Leptin Secretion.Environmental science & technology · 2026Article
- Loneliness associates with endothelial dysfunction in a community-based cohort: a pilot study and translational approach.NPJ cardiovascular health · 2025Article
- Clinical significance of elevated soluble T-cell immunoglobulin and mucin domain 1 and soluble P-selectin in individuals with obstructive sleep apnea-hypopnea syndrome.Saudi medical journal · 2023Article
- Sex Differences in Neurovascular Control: Implications for Obstructive Sleep Apnea.International journal of molecular sciences · 2023Review
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Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Obstructive sleep apnea (OSA) is an independent risk factor for cardiovascular disease. While intermittent hypoxia (IH) and catecholamine release play an important role in this increased risk, the mechanisms are incompletely understood. We have recently reported that IH causes endothelial cell (EC) activation, an early phenomenon in the development of cardiovascular disease, via IH-induced catecholamine release. Here, we investigated the effects of IH and epinephrine on gene expression in human aortic ECs using RNA-sequencing. We found a significant overlap between IH and epinephrine-induced differentially expressed genes (DEGs) including enrichment in leukocyte migration, cytokine-cytokine receptor interaction, cell adhesion and angiogenesis. Epinephrine caused higher number of DEGs compared to IH. Interestingly, IH when combined with epinephrine had an inhibitory effect on epinephrine-induced gene expression. Combination of IH and epinephrine induced MT1G (Metallothionein 1G), which has been shown to be highly expressed in ECs from parts of aorta (i.e., aortic arch) where atherosclerosis is more likely to occur. In conclusion, epinephrine has a greater effect than IH on EC gene expression in terms of number of genes and their expression level. IH inhibited the epinephrine-induced transcriptional response. Further investigation of the interaction between IH and epinephrine is needed to better understand how OSA causes cardiovascular 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.