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.
Exploring the role of epicardial adipose-tissue-derived extracellular vesicles in cardiovascular diseases / A.S. Rizzuto, G. Gelpi, A. Mangini, S. Carugo, M. Ruscica, C. Macchi. - In: ISCIENCE. - ISSN 2589-0042. - 27:4(2024 Apr 19), pp. 109359.1-109359.14. [10.1016/j.isci.2024.109359]
Exploring the role of epicardial adipose-tissue-derived extracellular vesicles in cardiovascular diseases
A.S. RizzutoPrimo
Writing – Original Draft Preparation
;S. CarugoWriting – Review & Editing
;M. Ruscica
Penultimo
Writing – Review & Editing
;C. MacchiUltimo
Writing – Review & Editing
2024
Abstract
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.File | Dimensione | Formato | |
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Alessandra Stefania Rizzuto.pdf
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