Exploring the role of epicardial adipose-tissue-derived extracellular vesicles in cardiovascular diseases
Alessandra Stefania Rizzuto,
Guido Gelpi,
Andrea Mangini,
Stefano Carugo,
Massimiliano Ruscica,
Chiara Macchi
Affiliations
Alessandra Stefania Rizzuto
Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy
Guido Gelpi
Department of Cardio-Thoracic-Vascular Diseases - Foundation IRCCS Cà Granda Ospedale Maggiore Policlinico, Milan, Italy
Andrea Mangini
Department of Cardio-Thoracic-Vascular Diseases - Foundation IRCCS Cà Granda Ospedale Maggiore Policlinico, Milan, Italy
Stefano Carugo
Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy; Department of Cardio-Thoracic-Vascular Diseases - Foundation IRCCS Cà Granda Ospedale Maggiore Policlinico, Milan, Italy
Massimiliano Ruscica
Department of Cardio-Thoracic-Vascular Diseases - Foundation IRCCS Cà Granda Ospedale Maggiore Policlinico, Milan, Italy; Department of Pharmacological and Biomolecular Sciences “Rodolfo Paoletti”, University of Milan, Milan, Italy; Corresponding author
Chiara Macchi
Department of Pharmacological and Biomolecular Sciences “Rodolfo Paoletti”, University of Milan, Milan, Italy
Summary: Epicardial adipose tissue (EAT) is a fat depot located between the myocardium and the visceral layer of the epicardium, which, owing to its location, can influence surrounding tissues and can act as a local transducer of systemic inflammation. The mechanisms upon which such influence depends on are however unclear. Given the role EAT undoubtedly has in the scheme of cardiovascular diseases (CVDs), understanding the impact of its cellular components is of upmost importance. Extracellular vesicles (EVs) constitute promising candidates to fill the gap in the knowledge concerning the unexplored mechanisms through which EAT promotes onset and progression of CVDs. Owing to their ability of transporting active biomolecules, EAT-derived EVs have been reported to be actively involved in the pathogenesis of ischemia/reperfusion injury, coronary atherosclerosis, heart failure, and atrial fibrillation. Exploring the precise functions EVs exert in this context may aid in connecting the dots between EAT and CVDs.
