Abstract
Atherothrombosis is the principal underlying cause of cardiovascular disease (CVD). Microvesicles (MV) are small blebs originated by an outward budding at the cell plasma membranes, which are released in normal conditions. However, MV release is increased in pathophysiologic conditions such as CVD. Low density lipoprotein (LDL) and MV contribute to atherothrombosis onset and progression by promoting inflammation and leukocyte recruitment to injured endothelium, as well as by increasing thrombosis and plaque vulnerability. Moreover, (oxidized)LDL induces MV release and vice-versa, perpetuating endothelium injury leading to CVD progression. Therefore, MV and lipoproteins exhibit common features, which should be considered in the interpretation of their respective roles in the pathophysiology of CVD. Understanding the pathways implicated in this process will aid in developing novel therapeutic approaches against atherothrombosis.
Highlights
Atherothrombosis is the principal underlying cause of cardiovascular disease (CVD)
MV and lipoproteins exhibit common features, which should be considered in the interpretation of their respective roles in the pathophysiology of CVD
The involvement of inflammation besides Low density lipoprotein (LDL) in atherosclerosis has been recently proven in the proof-of-concept CANTOS (Canakinumab Anti-Inflammatory Thrombosis Outcome Study) trial, showing that interleukin 1β inhibition resulted in a 15% reduction in cardiovascular events [12]
Summary
Atherosclerosis is caused by lipid accumulation associated with endothelial dysfunction and chronic low-grade inflammation and oxidative stress. Innate immunity cells and vascular smooth muscle cells respond to these perturbations by initiating interactions and gene programs that contribute to vascular dysfunction and atherosclerotic plaque formation. With a lipid-rich atheroma, show inward remodeling encroaching in the arterial lumen, which decrease blood flow, leading to tissue ischemia. Enhanced perivascular adipose tissue mass and local inflammation has been associated with increased atherosclerotic plaque burden [4], and immunity cells and inflammation have a causal role in atherosclerosis progression by modulating the resident cells in the artery wall [3]. Microvesicles (MV) derived from blood and vascular cells seem being able to participate in the initiation, progression and complications of atherothrombosis by a direct and a paracrine regulation of target cells. This review is aimed at summarizing the crosstalk between lipoproteins, inflammation, and microvesicles in the pathophysiology of atherothrombosis
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