Table 1.

Main findings about EVs in patients affected by COPD and in cellular or animal models if the disease.

Significance or Hypothesised Role for EVs	Source	Medium	Studied Population	References
Markers of endothelial apoptosis	Endothelium	Peripheral blood	COPD patients	[31, 32, 33, 36, 37]
Markers of endothelial dysfunction under stress	Endothelium	Peripheral blood	COPD patients	[43, 44]
Markers of disease severity	Endothelium Monocytes Neutrophils Endothelium	Peripheral blood BALF sputum	COPD patients	[38, 42] [52, 53] [56]
Markers of inflammation	Endothelium Monocytes Lymphocytes	Peripheral blood BALF	COPD patients	[36, 37, 38, 39] [54]
EV-miRNAs induce remodelling (myofibroblast transition from lung fibroblast)	n.a.	n.a. Peripheral blood	In vitro model Mixed model (human/murine)	[60] [46]
EVs induce emphysema-like disease	neutrophils	BALF	Mixed model (human/murine) Murine model	[51, 64] [63]
Protective role for EVs against inflammation	Mesenchymal cells	n.a. n.a.	In vitro model Murine model	[71] [72]
EVs as target of specific COPD treatments	Bronchial cells Endothelium	n.a.	In vitro model	[69]

EVs: extracellular vesicles; COPD: chronic obstructive pulmonary disease; BALF: bronchoalveolar lavage fluid; n.a.: not applicable.