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Smoking is a global risk factor for atherosclerosis, affecting societies all over the world. Smoking exerts its pro-atherogenic effects by triggering the generation of free radicals and by modifying vascular redox signaling. These abnormal vascular responses to cigarette smoking result into impaired endothelial function, decreased nitric oxide bioavailability, increased intima media thickness and finally atherosclerotic plaque formation in human arteries. Importantly, evidence suggests that cigarette smoking may have an effect on vascular smooth muscle cells function, leading to impaired endothelium-independent dilation in response to nitrate, in the brachial artery of healthy smokers. Taken together, it is now well established that smoking induces functional and structural abnormalities in the vascular wall, by mechanisms involving endothelial dysfunction and impairment of vascular smooth muscle cells in human arterial tree.

Original publication

DOI

10.1016/j.ijcard.2007.12.114

Type

Journal article

Journal

Int J Cardiol

Publication Date

18/08/2008

Volume

128

Pages

151 - 153

Keywords

Asian Continental Ancestry Group, Atherosclerosis, Endothelium, Vascular, Humans, Muscle, Smooth, Vascular, Oxidation-Reduction, Oxidative Stress, Signal Transduction, Smoking