Key result
Microvesicles and LDL mutually drive release to accelerate inflammation, leukocyte recruitment, and thrombosis.
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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.
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Chiva‐Blanch et al. (2019) conducted a review in Cardiovascular disease / Atherothrombosis. Microvesicles and lipoproteins was evaluated. Microvesicles and low-density lipoproteins mutually induce release and promote inflammation, leukocyte recruitment, and thrombosis in atherothrombosis progression.
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