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Related Experiment Video

Updated: Aug 24, 2025

Generation of Electronic Cigarette Aerosol by a Third-Generation Machine-Vaping Device: Application to Toxicological Studies
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Chronic E-Cigarette Use Impairs Endothelial Function on the Physiological and Cellular Levels.

Leila Mohammadi1, Daniel D Han1,2, Fengyun Xu3

  • 1Division of Cardiology (L.M., D.D.H., R.D., P.R., P.G., M.L.S.), University of California, San Francisco.

Arteriosclerosis, Thrombosis, and Vascular Biology
|October 26, 2022
PubMed
Summary
This summary is machine-generated.

Chronic e-cigarette use impairs vascular function, reducing nitric oxide release and increasing endothelial permeability. Vaping may also uniquely affect oxidative stress, with a potential role for RAGE in these harmful vascular effects.

Keywords:
biomarkercell adhesionendothelial cellinflammationligand

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Area of Science:

  • Cardiovascular Research
  • Endothelial Biology
  • Toxicology

Background:

  • Established vascular harm from smoking.
  • Limited understanding of chronic e-cigarette effects on endothelial function.

Purpose of the Study:

  • Hypothesize e-cigarette use alters blood milieu, impairing endothelial function.
  • Investigate vascular effects of chronic e-cigarette use.

Main Methods:

  • Measured endothelial function (flow-mediated dilation) in e-cigarette users, smokers, and nonusers.
  • Assessed effects of participant sera and e-cigarette aerosol on endothelial cells (NO, H2O2 release, permeability).

Main Results:

  • E-cigarette users and smokers showed lower flow-mediated dilation.
  • Sera from users/smokers reduced nitric oxide secretion; e-cigarette user sera increased endothelial permeability and H2O2 release.
  • Distinct biomarker profiles for inflammation, thrombosis, and cell adhesion were observed.

Conclusions:

  • Chronic vaping and smoking impair endothelial function and nitric oxide release.
  • Vaping uniquely increases microvascular endothelial permeability and may affect oxidative state.
  • Receptor for advanced glycation end products (RAGE) implicated in e-cigarette-induced endothelial changes.