Hydroperoxides and cytokines as biomarkers in detecting atherosclerosis predisposition in cigarette smokers

Abstract

Objectives: Smoking increases oxidative modi-fication of LDL, associated with lower HDL plasma levels, systemic inflammatory response and endothelial dysfunction. We tested the hy-pothesis that the risk status for coronary atherosclerosis disease (CAD) of cigarettes smokers might be identified by means of serum oxidative levels and vascular inflammation de-termination. Design and Methods: Oxidative stress levels, cytokines, and the metabolic status were investigated on 499 subjects admit-ted to our institute. The association between biomarkers and smoking habits in the pres-ence/absence of disease and with the number of vessel affected, was studied. Results: Oxidative stress and inflammatory levels (p < 0.001) were strongly induced by smoking habits. Serum values of the subjects categorised as CAD, non CAD and healthy subjects differed significantly (p < 0.001) only for the degree of oxidative stress. Glycaemia was able to affect C-reactive protein serum levels with a positive association (p < 0.05). The analysis of the study population in-dicated that serum oxidative stress levels sig-nificantly increased with increasing number of vessels affected (p < 0.01). When statistical analysis was performed separately in both smoking groups, smokers did not show any particular difference for both oxidative stress and inflammation markers between the two groups of cardiovascular patients (CAD and non CAD) and the control group, while for non smokers, the differences were evident. Conclu-sion: These findings indicate that the consid-ered biomarkers, especially oxidative stress, can be useful to predict the biological damage caused by cigarette smoking, as well as to iden-tify subjects characterised by a higher risk of cardiovascular event, but cannot evaluate the presence of disease in subjects with smoking habit

Atherosclerosis and Toll-Like Receptor4 (TLR4), Lectin-Like Oxidized Low-Density Lipoprotein-1 (LOX-1), and Proprotein Convertase Subtilisin/Kexin Type9 (PCSK9)

“…Importantly, LOX-1 is also expressed in atheroma-derived of human and animal atherosclerotic lesions. The expression of LOX-1 is induced by several pro-inflammatory cytokines (TNF- α , IL-1, IFN- γ ), CRP, LPS, modified lipoproteins, hypertension-related stimuli (angiotensin II, endothelin-1, and fluid shear stress), hyperglycemic stimuli (high glucose and AGEs), IL-6, and some other stimuli-like homocysteine and free radicals [ 48 , 61 – 63 ]. Pathological conditions such as diabetes mellitus, hypertension, hyperlipidemia, myocardial ischemia, and atherosclerosis are associated with an induction in LOX-1 expression.…”

Atherosclerosis and Toll-Like Receptor4 (TLR4), Lectin-Like Oxidized Low-Density Lipoprotein-1 (LOX-1), and Proprotein Convertase Subtilisin/Kexin Type9 (PCSK9)

“…Importantly, LOX-1 is also expressed in atheroma-derived of human and animal atherosclerotic lesions. The expression of LOX-1 is induced by several pro-inflammatory cytokines (TNF- α , IL-1, IFN- γ ), CRP, LPS, modified lipoproteins, hypertension-related stimuli (angiotensin II, endothelin-1, and fluid shear stress), hyperglycemic stimuli (high glucose and AGEs), IL-6, and some other stimuli-like homocysteine and free radicals [ 48 , 61 – 63 ]. Pathological conditions such as diabetes mellitus, hypertension, hyperlipidemia, myocardial ischemia, and atherosclerosis are associated with an induction in LOX-1 expression.…”

Atherosclerosis and Toll-Like Receptor4 (TLR4), Lectin-Like Oxidized Low-Density Lipoprotein-1 (LOX-1), and Proprotein Convertase Subtilisin/Kexin Type9 (PCSK9)

“…Importantly, LOX-1 is also expressed in atheroma-derived of human and animal atherosclerotic lesions. The expression of LOX-1 is induced by several pro-inflammatory cytokines (TNF- α , IL-1, IFN- γ ), CRP, LPS, modified lipoproteins, hypertension-related stimuli (angiotensin II, endothelin-1, and fluid shear stress), hyperglycemic stimuli (high glucose and AGEs), IL-6, and some other stimuli-like homocysteine and free radicals [ 48 , 61 – 63 ]. Pathological conditions such as diabetes mellitus, hypertension, hyperlipidemia, myocardial ischemia, and atherosclerosis are associated with an induction in LOX-1 expression.…”

Atherosclerosis and Toll-Like Receptor4 (TLR4), Lectin-Like Oxidized Low-Density Lipoprotein-1 (LOX-1), and Proprotein Convertase Subtilisin/Kexin Type9 (PCSK9)

“…Importantly, LOX-1 is also expressed in atheroma-derived of human and animal atherosclerotic lesions. The expression of LOX-1 is induced by several pro-inflammatory cytokines (TNF- α , IL-1, IFN- γ ), CRP, LPS, modified lipoproteins, hypertension-related stimuli (angiotensin II, endothelin-1, and fluid shear stress), hyperglycemic stimuli (high glucose and AGEs), IL-6, and some other stimuli-like homocysteine and free radicals [ 48 , 61 – 63 ]. Pathological conditions such as diabetes mellitus, hypertension, hyperlipidemia, myocardial ischemia, and atherosclerosis are associated with an induction in LOX-1 expression.…”