In hypercholesterolemic patients, exercise training on top of rosuvastatin treatment lead to a small, but significant decrease in the proportion of inflammatory monocytes. Here we could demonstrate that monocyte subsets were not associated with statin treatment and that the association between sdLDL and monocyte subset distribution was independent of statin treatment dose. In addition, we demonstrated that sdLDL plasma levels exhibit no association with circulating pro- and anti-inflammatory markers, namely hsCRP, IL-6, IL-10 and TNF-��. This is in line with previously published literature, as in the Quebec Cardiovascular Study cohort including 2025 men free of CAD at baseline, sdLDL levels only marginally correlated with markers of inflammation such as hsCRP. In the literature, non-classical monocytes were defined as a major source of TNF. In a study comparing patients with coronary artery disease and apparently disease-free subjects, though mixing acute MI patients and stable CAD patients, TNF-�� showed a correlation with non-classical monocytes in a model with only two monocyte subsets. Severely injured patients showed a correlation between CRP levels and the intermediate subset, a possible cellular hallmark of acute illness. In patients with acute erysipelas, CRP and IL-6 levels correlated with an inflammatory monocyte subset. However, these cells exhibited reduced intracellular TNF protein as compared to classical monocytes. This highlights the complex and far from fully understood mechanisms of inflammatory cytokine production in monocyte subsets KRX-0401 during inflammatory activation. Interestingly, besides a weak correlation between hsCRP and intermediate monocytes, no correlations between circulating inflammatory markers and monocyte subsets were shown in our study population. Therefore one may speculate that elevated plasma levels of sdLDL exert some of its detrimental effects via modulation of monocyte subset distribution to a rather pro-inflammatory and pro-WZ4002 atherogenic profile, rather than directly influencing classical inflammatory pathways. Some limitations of the present study have to be acknowledged. First, this is a single center study with a rather small number of patients. Furthermore, the cross-sectional study design only allows us to outline associations between monocyte subset distribution and LDL subfractions, while we cannot draw functional insights into monocyte subset plasticity in atherosclerotic disease. In addition, we did not include a control group with absence of coronary stenosis at coronary angiography. This would be of particular interest, as the absence of low-grade vascular inflammation would help to assess possible direct effects of sdLDL on monocytes. However, our results indicate a link between innate immunity and lipid metabolism in stable atherosclerosis. In conclusion, this study provides evidence for the first time for an association between plasma levels of atherogenic sdLDL particles and an increased proportion of non-classical monocytes and a smaller classical monocyte population. Thioredoxin reductase is a homodimetric protein essential for reduction and activation of Trx, each subunit of which has a redox active disulfide/dithiol and a tightly bound flavin adenine dinucleotide group that could mediate the transfer of reducing equivalents from NADPH to a disulfide bond of the substrates. The inhibition of both cytosolic and mitochondrial TrxR can affect the intracellular redox balance and hence alter the mitochondrial membrane permeability and consequent release of the segregated proapoptotic factors, finally resulting in apoptosis of cancer cells.