Abstract
Cigarette smoking is a risk factor for the development of peripheral artery disease (PAD), although the proatherosclerotic mediators of cigarette smoking are not entirely known. We explored whether circulating microRNAs (miRNAs) are dysregulated in cigarette smokers and associated with the presence of PAD. Ninety-four participants were recruited, including 58 individuals without and 36 with PAD, 51 never smokers, 28 prior smokers, and 15 active smokers. The relative expression of six circulating miRNAs with distinct biological roles (miR-21, miR-27b, miR-29a, miR-126, miR-146, and miR-218) was assessed. Cigarette smoking was associated with the presence of PAD in multivariate analysis. Active smokers, but not prior smokers, presented miR-27b downregulation and higher leukocyte, neutrophil, and lymphocyte counts; miR-27b expression levels were independently associated with active smoking. Considering the metabolic and/or inflammatory abnormalities induced by cigarette smoking, miR-27b was independently associated with the presence of PAD and downregulated in patients with more extensive PAD. In conclusion, the atheroprotective miR-27b was downregulated in active smokers, but not in prior smokers, and miR-27b expression was independently associated with the presence of PAD. These unreported data suggest that the proatherogenic properties of cigarette smoking are mediated by a downregulation of miR-27b, which may be attenuated by smoking cessation.
Highlights
Patients with peripheral artery disease (PAD) presented a higher prevalence of classical cardiovascular risk factors, concomitant coronary and carotid artery disease, and use of antiplatelet and statin therapy, as well as higher creatinine levels, compared to patients without PAD
The ∆Cycle threshold (Ct) miR-27b and ∆Ct miR-146 values were significantly higher in patients with PAD (Table 1), corresponding to a 17.0- and 3.4-fold downregulation of miR-27b and miR-146 [38], respectively, in patients with PAD
27b was significantly downregulated in active smokers compared with prior smokers but with never smokers, therewith wasthe a trend towards miR-27b downregulation in
Summary
Cigarette smoking is a major health hazard, being accountable for substantial cardiovascular morbidity and mortality worldwide due to its proatherogenic effects [1]. Cigarette smoking increases the risk of atherosclerosis development by several fold and is a more influential risk factor for peripheral artery disease (PAD) than for atherosclerosis of other territories, including coronary arteries [2]. Some of the mechanisms associated with cigarette-smoking-induced atherogenesis include the activation of inflammation, dysregulation of the lipid metabolism, increase in oxidative stress, and endothelial dysfunction [1,2]. The pathophysiology associated with the initiation and progression of atherosclerosis secondary to cigarette smoking is not entirely known [1,2]
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