Evidence map›Paper›PMID 37369447›Full record

ArticleAlcohol, clinical & experimental research2023

Alcohol and vascular endothelial function: Biphasic effect highlights the importance of dose.

Naresh K Rajendran, Weimin Liu, Paul A Cahill, Eileen M Redmond

Open access · greenAbstract read
In one paragraph

Article in Alcohol, clinical & experimental research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.1field-weighted citation impact, top 9% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 12 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Alcohol Metabolism into Acetaldehyde in Developing Cerebral Arteries.International journal of molecular sciences · 2026
    Article
  6. Sigma-1 receptors, alcohol consumption, and arterial tone: a new intersection in cardiovascular physiology.American journal of physiology. Heart and circulatory physiology · 2026
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Naresh K RajendranDepartment of Surgery, University of Rochester Medical Center, Rochester, New York, USA.ORCID https://orcid.org/0000-0003-4401-6912
Weimin LiuDepartment of Surgery, University of Rochester Medical Center, Rochester, New York, USA.
Paul A CahillVascular Biology and Therapeutics Laboratory, School of Biotechnology, Dublin City University, Dublin, Ireland.ORCID https://orcid.org/0000-0002-5385-6502
Eileen M RedmondDepartment of Surgery, University of Rochester Medical Center, Rochester, New York, USA.ORCID https://orcid.org/0000-0001-8642-4418
University of Rochester Medical Center · USDublin City University · IE

Funding

Vascular Protective Effects of Alcohol - Role of NotchR01AA024082 · NIAAA · UNIVERSITY OF ROCHESTER · PI REDMOND, EILEEN M. · 2018 to 2021
$1.4M
NIAAA NIH HHS R01 AA024082NIH HHS R01 AA024082
6 · The paper itself

Abstract

backgroundAlcohol (ethanol) consumption has different influences on arterial disease, being protective or harmful depending on the amount and pattern of consumption. The mechanisms mediating these biphasic effects are unknown. Whereas endothelial cells play a critical role in maintaining arterial health, this study compared the effects of moderate and high alcohol concentrations on endothelial cell function.

methodsHuman coronary artery endothelial cells (HCAEC) were treated with levels of ethanol associated with either low-risk/moderate drinking (i.e., 25 mM) or high-risk/heavy drinking (i.e., 50 mM) after which endothelial function was assessed. The effect of ethanol's primary metabolite acetaldehyde (10 and 25 μM) was also determined.

resultsModerate ethanol exposure (25 mM) improved HCAEC barrier integrity as determined by increased transendothelial electrical resistance (TEER), inhibited cell adhesion molecule (CAM) mRNA expression, decreased inflammatory cytokine (interferon-γ and interleukin 6) production, inhibited monocyte chemotactic protein-1 (MCP-1) expression and monocyte adhesion, and increased homeostatic Notch signaling. In contrast, exposure to high-level ethanol (50 mM) decreased TEER, increased CAM expression and inflammatory cytokine production, and stimulated MCP-1 and monocyte adhesion, with no effect on Notch signaling. Reactive oxygen species (ROS) generation and endothelial nitric oxide synthase activity were increased by both alcohol treatments, and to a greater extent in the 50 mM ethanol group. Acetaldehyde-elicited responses were generally the same as those of the high-level ethanol group.

conclusionsEthanol has biphasic effects on several endothelial functions such that a moderate level maintains the endothelium in a nonactivated state, whereas high-level ethanol causes endothelial dysfunction, as does acetaldehyde. These data show the importance of dose when considering ethanol's effects on arterial endothelium, and could explain, in part, the J-shaped relationship between alcohol concentration and atherosclerosis reported in some epidemiologic studies.

Indexed as

alcoholatherosclerosisendothelialvascular

Identifiers

PMID37369447
PMCPMC10751391
OpenAlexW4382199127

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.