Inflammatory Mediators of Platelet Activation: Focus on Atherosclerosis and COVID-19.
Int J Mol Sci
; 22(20)2021 Oct 16.
Article
in English
| MEDLINE | ID: covidwho-1470892
ABSTRACT
BACKGROUND:
Atherosclerotic cardiovascular diseases are characterized by a dysregulated inflammatory and thrombotic state, leading to devastating complications with increased morbidity and mortality rates.SUMMARY:
In this review article, we present the available evidence regarding the impact of inflammation on platelet activation in atherosclerosis. Key messages In the context of a dysfunctional vascular endothelium, structural alterations by means of endothelial glycocalyx thinning or functional modifications through impaired NO bioavailability and increased levels of von Willebrand factor result in platelet activation. Moreover, neutrophil-derived mediators, as well as neutrophil extracellular traps formation, have been implicated in the process of platelet activation and platelet-leukocyte aggregation. The role of pro-inflammatory cytokines is also critical since their receptors are also situated in platelets while TNF-α has also been found to induce inflammatory, metabolic, and bone marrow changes. Additionally, important progress has been made towards novel concepts of the interaction between inflammation and platelet activation, such as the toll-like receptors, myeloperoxidase, and platelet factor-4. The accumulating evidence is especially important in the era of the coronavirus disease-19 pandemic, characterized by an excessive inflammatory burden leading to thrombotic complications, partially mediated by platelet activation. Lastly, recent advances in anti-inflammatory therapies point towards an anti-thrombotic effect secondary to diminished platelet activation.Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Inflammation Mediators
/
Atherosclerosis
/
COVID-19
Limits:
Humans
Language:
English
Year:
2021
Document Type:
Article
Affiliation country:
Ijms222011170
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