Nicotine: A Double-Edged Sword in Atherosclerotic Disease.
Chronic cigarette smoking is well-known to damage vascular endothelium, which initiates atherosclerosis by first manifesting as endothelial dysfunction and later progressing to cardiovascular diseases (CVD). Nicotine, a major component of tobacco smoke, is traditionally thought to be responsible for increased cardiovascular events through stimulation of the sympathetic nervous system, increased myocardial metabolic demand, impaired lipid metabolism, and activated platelet function. However, recent studies have demonstrated that nicotine, at lower doses, may be beneficial to the cardiovascular system. With binding to specific nicotinic acetylcholine receptors, nicotine can induce migration and proliferation of vascular cells, and hence enhances angiogenesis. Therefore, these seemingly inconsistent properties of nicotine may in fact give rise to novel and efficacious management strategies of CVD.


BACKGROUND
Angiogenesis; Atherosclerosis; nicotinic acetylcholine receptors (nAChRs); Nicotine.
Section of Cardiology, Department of Internal Medicine, Mackay Memorial Hospital, Mackay Medical College, Taipei, Taiwan; ; Institute of Biomedical Sciences, Mackay Medical College, New Taipei City, Taiwan;
Chun-Chieh
CC
Liu
Section of Cardiology, Department of Internal Medicine, Mackay Memorial Hospital, Mackay Medical College, Taipei, Taiwan; ; Institute of Biomedical Sciences, Mackay Medical College, New Taipei City, Taiwan; ; Department of Medicine, Mackay Medical College, New Taipei City, Taiwan.
Hung-I
HI
Yeh