Abstract
Monocytes play a key role in cardiovascular disease (CVD) as their influx into the vessel wall is necessary for the development of an atherosclerotic plaque. Monocytes are, however, heterogeneous differentiating from classical monocytes through the intermediate subset to the nonclassical subset. While it is recognized that the percentage of intermediate and nonclassical monocytes are higher in individuals with CVD, accompanying changes in inflammatory markers suggest a functional impact on disease development that goes beyond the increased proportion of these ‘inflammatory’ monocyte subsets. Furthermore, emerging evidence indicates that changes in monocyte proportion and function arise in dyslipidemia, with lipid lowering medication having some effect on reversing these changes. This review explores the nature and number of monocyte subsets in CVD addressing what they are, when they arise, the effect of lipid lowering treatment, and the possible implications for plaque development. Understanding these associations will deepen our understanding of the clinical significance of monocytes in CVD.
Highlights
Assessment of monocyte numbers reveals that the proportions of the three subsets are perturbed in Cardiovascular disease (CVD) and associate with disease severity, the occurrence and outcomes of clinical events, and plaque progression
While elevation of the intermediate and nonclassical subsets suggests that their ascribed inflammatory functions contribute to atherosclerosis, it is important to consider the broader functional changes both within the subsets and across the whole monocyte population, that occur in CVD
Of specific relevance to atherosclerosis are increased inflammation and migration. These cellular changes are observed in association with specific lipids, high density lipoprotein (HDL)-C, indicating that lipids may influence both monocyte subset proportions and function
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The main etiological factor for CVD is atherosclerosis which principally affects the coronary, as well as the cerebrovascular and peripheral circulation, with risk of heart attack, stroke and limb loss. Carotid artery disease can be asymptomatic, but progressive and unstable plaque carries a significant risk of stroke. Risk factors for CVD are broadly considered either non-modifiable (e.g., age, sex, family history of premature CVD) or modifiable (e.g., hypercholesterolemia, hypertension, tobacco smoking, overweight or obesity, insulin resistance or diabetes, lack of physical activity). Addressing these modifiable risk factors could prevent or delay the atherosclerotic process [5]. Dyslipidemias are considered key contributors to the development of atherosclerotic plaque. The monocyte alterations of relevance to CVD, and dyslipidemia, will be the focus of this review, with a discussion of more recent insight into how these changes may be promoting plaque progression
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