Smoking cessation and vascular endothelial function

Abstract

Smoking is associated with vascular endothelial dysfunction. It is thought that smoking impairs vascular endothelial function through a decrease in nitric oxide bioavailability induced by activation of oxidative stress and inflammation. Endothelial dysfunction can be improved or augmented by appropriate interventions including pharmacotherapy, administration of supplements and lifestyle modifications. Although there have not been many studies, the effects of smoking cessation on endothelial function have been shown. In those studies, it was shown that smoking cessation does not always have a positive effect on vascular endothelial function. In this review, I will focus on the role of smoking in endothelial function and the effects of smoking cessation on endothelial function.

In Association with Other Risk Factors, Smoking Is the Main Predictor for Lower Transcutaneous Oxygen Pressure in Type 2 Diabetes

“…Cigarette smoke directly damages cellular and sub-cellular structures via reactive oxygen and nitrogen species and the resulting oxidative stress [57]. Smoking causes vascular wall contraction by activating Rho kinase, promoting monocyte adhesion to endothelial cells and entering monocytes and macrophages into endothelium [58,59]. Nicotine from cigarette smoke causes migration, proliferation, apoptosis, phenotypic changes, and the contraction of smooth muscle cells in the arterial wall [60].…”

Smoking-Induced DNA Hydroxymethylation Signature Is Less Pronounced than True DNA Methylation: The Population-Based KORA Fit Cohort

“…Epigenetic mechanisms, specifically alterations in DNA methylation, have been suggested to moderate the impact of tobacco smoking, leading to changes in transcriptional activity and contributing to smoking-related diseases [ 9 ]. With the update of DNA methylation arrays, the impact of smoking on DNA 5-methylcytosine (5mC) methylation has been thoroughly investigated in blood cells from adults, revealing significant disparities between smokers and non-smokers [ 10 , 11 ], which can be even more conspicuous in specific tissues like vascular endothelial cells [ 12 ], and vulnerable groups like cancer patients [ 4 ]. The impact of tobacco smoking on DNA methylation is also prominent in the blood of newborns whose mothers smoked during pregnancy [ 13 ].…”