Extracellular Vesicles as Drivers of Immunoinflammation in Atherothrombosis
Abstract
:1. Introduction
2. Extracellular Vesicles: Current State and Emerging Concepts
3. EVs as Pathophysiological Drivers of Atherothrombosis
3.1. Atherogenesis
3.2. Atheroinflammation
3.3. Lesion Progression
3.3.1. Atherogenic Foam Cell Formation
3.3.2. Vascular Smooth Muscle Cell Proliferation, Migration, and Phenotype Switching
3.3.3. Intravascular Calcification
3.3.4. Necrotic Core
3.4. Advanced Lesion and Plaque Rupture
3.4.1. Arterial Neoangiogenesis and Intraplaque Hemorrhage
3.4.2. Thrombus Formation after Rupture
4. Extracellular Vesicles as Diagnostic and Prognostic Biomarkers
Clinical Condition/Context | EV Subtype | Cargo | Reference |
---|---|---|---|
Cardiovascular risk factors | ↑ eEV (CD144+, CD105+) (Hypertension) | [267] | |
↑ lEV (CD3+) (Hypertension) | [235] | ||
↑ eEV (CD31+/42−; CD31+/AnnV+), pEV (CD31+/42+) (Diabetes) | miR-126 | [236] | |
↑ lEV (CD45+), nEV (CD15+), pEV (CD62P+) (Familial hypercholesterolemia [FH]) | [242] | ||
↑ pEV (CD42a+, CD62P+) (Obesity) | [268] | ||
↑ pEV (CD41+), eEV (CD62E+), lEV (CD45+) (Smoking) | CD40L | [269] | |
Pulmonary hypertension | ↑ eEV (CD31+, CD144+, CD62E+), lEV (CD45+) | [260] | |
Endothelial dysfunction | eEV (CD31+/CD42b−) | [255] | |
eEV (CD31+/AnnV+) | [256] | ||
FH and subclinical atherosclerosis | ↑ lEV (CD3+/CD45+) | [50] | |
↑ pEV (TSP1+/CD142+) | Tissue factor | [266] | |
Coronary artery disease (CAD) | ↑ CD31+/Annexin V+ EV | [258] | |
↑ eEV (CD31+), pEV (CD42b+) | miR-126, miR-199a | [241] | |
↑ eEV (CD31+/AnnV+) | [256] | ||
↑ eEV (CD31+ and CD51+) | [238] | ||
↑ eEV (CD31+) | [270] | ||
Arterial hypertension and coronary artery disease | ↑ eEV (CD31+/41−, CD62E+, CD144+) | [271] | |
Diabetes and CAD | ↑ eEV (CD62E+, CD31+) | ↓LAP(TGF-β1), PD-ECGF, PF4, TSP1 | [233] |
Coronary heart disease | ↑ eEV (CD31+/CD42−, CD144+) | [272] | |
↑ pEV (CD41+), eEV (CD144+) | [273] | ||
↑ eEV (CD31+ and CD146+) | [248] | ||
Stable angina | ↑ eEV (CD31+), pEV (CD41+) | [274] | |
Acute coronary syndrome | ↑ pEV (CD31+, CD41a+) | [275] | |
↑ eEV (CD146+) | [276] | ||
↑ eEV (CD144+), ErEV (CD235a+), pEV (CD41a+) | [261] | ||
Myocardial infarction (MI) | ↑ CM-EV and eEV (CD31+/CD41−) | Caveolin-3, TnT | [185] |
↑ ErEV (CD235a+) | [207,252] | ||
↑ eEV (CD144+) | [277] | ||
↑ l/mEV, eEV, ErEV, activated vascular cell-EV, (CD66b+/62E+/142+ for coronary thrombosis) | [245] | ||
↑ eEV (CD154+, CD62E+), pEV (CD62P+) | [278] | ||
↑ eEV (CD31+), pEV (GPIbα) | [247] | ||
↑ eEV (CD31+, CD146+), pEV (CD42b+) | [254] | ||
↑ pEV (CD61+), mEV (CD14+) | Tissue factor | [244] | |
↑ lEV(CD45+), pEV (CD61/62P+), ErEV (CD235a+) | Lactadherin, Fbn | [279] | |
↑ eEV (CD144+), pEV (CD62P+/41), mEV (CD14+) | Tissue factor | [280] | |
MI and stable angina | ↑ pEV (CD51+/61+), eEV (CD42−/31+), mEV (CD14+) | Tissue factor | [250] |
MI in chronic kidney disease | ↑ eEV (CD154+, CD62E+), pEV (CD62P+) | [278] | |
Ischemic cerebrovascular disease | ↑ eEV (CD144+, CD31+, CD62E+/41a−, AnnV+) | [281] | |
↑ eEV (CD62E+, CD31+/, CD42b− and Annexin V+) | [237] | ||
Stroke | ↑ NPC-EV (CD34+, CD56+) | [282] | |
↑ pEV (CD41+) | [283] | ||
↑ eEV (CD62E+) | [259] | ||
↑ eEV (CD31+, CD144+, CD146+), lEV (CD45+) | [243] | ||
Peripheral arterial disease | ↑ pEV (CD41+/61+) | Calprotectin | [284] |
↑ cEV | Sonic hedgehog | [285] | |
↑ eEV (CD144+) | [286] | ||
Venous thromboembolism | ↑ eEV (CD62E+), mEV (CD14+) | PSGL-1+ | [287] |
Atrial fibrillation and stroke | ↑ eEV (CD41−/31+), pEV (CD61+) | [288] | |
Autoimmune chronic inflammatory diseases | ↑ eEV and pEV | [289] |
Pharmacological Modulation of Extracellular Vesicles
5. Extracellular Vesicles as Therapeutic Tools
6. Future Perspectives and Conclusions
Author Contributions
Funding
Acknowledgments
Conflicts of Interest
References
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Suades, R.; Greco, M.F.; Padró, T.; Badimon, L. Extracellular Vesicles as Drivers of Immunoinflammation in Atherothrombosis. Cells 2022, 11, 1845. https://doi.org/10.3390/cells11111845
Suades R, Greco MF, Padró T, Badimon L. Extracellular Vesicles as Drivers of Immunoinflammation in Atherothrombosis. Cells. 2022; 11(11):1845. https://doi.org/10.3390/cells11111845
Chicago/Turabian StyleSuades, Rosa, Maria Francesca Greco, Teresa Padró, and Lina Badimon. 2022. "Extracellular Vesicles as Drivers of Immunoinflammation in Atherothrombosis" Cells 11, no. 11: 1845. https://doi.org/10.3390/cells11111845