Table 4.
Study | EV Biomarkers | EV Cellular Origin | Study Findings | Reference |
---|---|---|---|---|
Daniel, L.; et al. | proteinase 3 (PR3), myeloperoxidase (MPO) |
EV released from primed neutrophils in vitro | EV can induce endothelial activation, ROS production, cytokines release |
[91] |
Brogan, P.A.; et al. | Platelets, neutrophils, endothelial cells |
EV level increased in vasculitis Decrease of neutrophil-derived EV after treatment Endothelial-derived EV correlated with disease activity |
[92] | |
Kahn, R.; et al. | B1 kinin receptor | Leukocytes | EV level increased in vasculitis Neutrophil-derived B1+ EV found on glomerular endothelial cells and renal injury |
[93] |
Prikryl, P.; et al. | Urinary EV | Proteomic EV profiling showed different regulation of proteins potentially involved in vasculitis pathogenesis | [94] | |
Surmiak, M.; et al. | leukotriene (LT)B4, 5-oxo-eicosatetraenoic acid (5-oxo-ETE) |
EV enriched in LTB4 and 5-oxo-ETE in granulomatosis with polyangiitis | [95] | |
Wang, Y.; et al. | Sequencing analysis of EV miRNA cargo in microscopic polyangiitis identified a correlation between miR-185-3p, miR-125a-3p and both the clinical activity score and proteinuria | [97] | ||
Manojlovic, M.; et al. | myeloperoxidase (MPO), PTX3, high mobility group box 1 (HMGB1) | PTX3+ and HMGB1+ EV correlated with disease activity HMGB1 potentially associated with renal injury |
[98] | |
Antovic, A.; et al. | myeloperoxidase (MPO), C3a, C5a | MPO C3a+ and C5a+ EV increased in vasculitis, particularly in patients with renal involvement C3a and C5a expressed on EV correlated with disease activity |
[100] | |
Miao, D.; et al. | chemokines, adhesion molecules, growth and apoptotic factors | Platelets | Increased EV in vasculitis EV correlate with disease activity and renal injury |
[101] |