Abstract
Extracellular vesicles (EVs) have emerged as a novel intercellular communication system. By carrying bioactive lipids, miRNAs and proteins they can modulate target cell functions and phenotype. Circulating levels of EVs are increased in inflammatory conditions, e.g., cardiovascular disease patients, and their functional contribution to atherosclerotic disease development is currently heavily studied. This review will describe how EVs can modulate vascular cell functions relevant to vascular inflammation and atherosclerosis, particularly highlighting the role of EV-associated proteolytic activity and effector proteins involved. Furthermore, we will discuss key questions and challenges, especially for EV-based therapeutics.
Highlights
INTRODUCTIONExtracellular vesicles (EVs) play a crucial physiological and pathophysiological role, as they have been identified as regulators of cell-to-cell communication [1]
Extracellular vesicles (EVs) play a crucial physiological and pathophysiological role, as they have been identified as regulators of cell-to-cell communication [1].Extracellular vesicles are small spherical vesicles, consisting of a lipid bilayer membrane encasing a small organelle-free cytosol, that are released by cells into the extracellular environment [2]
This review will give a brief overview on how EVs can modulate vascular cell functions relevant to vascular inflammation and atherosclerosis, highlighting the role of EV-associated proteolytic activity and effector proteins involved
Summary
Extracellular vesicles (EVs) play a crucial physiological and pathophysiological role, as they have been identified as regulators of cell-to-cell communication [1]. EVs are generally classified into three main classes, i.e., exosomes, microvesicles (MVs), and apoptotic bodies [3]. Exosomes arise from intracellular compartments called multivesicular bodies (MVBs) and are released by an active process, leading to fusion of these MVBs with the plasma membrane [4]. The second class of EVs is MVs, which are typically larger in size (ranging from 100 to 1,000 nm) and are produced by budding off directly from the plasma membrane in a process called microvesiculation [5]. The third type of EVs is apoptotic bodies with a size of >1 μm These vesicles are released from apoptotic cells through membrane blebbing and contain apoptotic nuclear material [9]. Frontiers in Cardiovascular Medicine | www.frontiersin.org van der Vorst et al
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
