Molecular Linkage between Atherosclerosis and Extracellular Vesicles

Dear Colleagues,

Atherosclerosis is a chronic inflammatory disease driven by lipid accumulation in arteries, leading to narrowing and thrombosis that cause mortality. Atherosclerosis affects younger people and is involved in the majority of deaths worldwide. Vascular inflammation contributes to atherogenesis by activation of the molecular and cellular pathways and plays a critical role in causing atherosclerosis plaques to become unstable and rupture, leading to a stroke or myocardial infarction. The molecular mechanisms associated with thrombotic complications of atherosclerosis have evolved much beyond the ‘vulnerable plaque’ concept. Extracellular vesicles (EVs), like exosomes, are small, lipid bilayer-enclosed structures secreted by endothelial cells, immune cells and other cardiovascular tissues. They are associated with key steps in atherosclerosis, including endothelial dysfunction and vascular wall inflammation resulting in vascular remodeling. EVs inherit bioactive components from parent cells and are able to transfer their contents to recipient cells. EVs regulate gene expression in recipient cells by carrying mRNA, miRNA, proteins and bioactive molecules between cells. EV microRNAs are key players in cardiac regeneration and have cardioprotective and regenerative properties that influence cardiac and non-cardiac cells as well as stem and progenitor cells. Therefore, EVs are valuable prognostic and diagnostic biomarkers and therapeutic targets in cardiovascular diseases.

Dr. Wioletta Olejarz
Guest Editor

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