Soluble platelet selectin and platelets in COVID-19: a multifaceted connection.
COVID-19
platelet
soluble platelet selectin
Journal
Annals of medicine and surgery (2012)
ISSN: 2049-0801
Titre abrégé: Ann Med Surg (Lond)
Pays: England
ID NLM: 101616869
Informations de publication
Date de publication:
Aug 2024
Aug 2024
Historique:
received:
11
04
2024
accepted:
13
06
2024
medline:
9
8
2024
pubmed:
9
8
2024
entrez:
9
8
2024
Statut:
epublish
Résumé
The COVID-19 pandemic has brought to light the intricate relationship between platelets, soluble platelet selectin (sP-selectin), and disease pathogenesis. Platelets, traditionally recognized for their role in hemostasis, have emerged as key contributors to the immunothrombotic complications observed in COVID-19 patients. Concurrently, elevated levels of sP-selectin, indicative of platelet activation and endothelial injury, have been consistently identified in COVID-19 patients and have shown associations with disease severity and adverse outcomes. This multifaceted connection underscores the pivotal role of platelets and sP-selectin in orchestrating thromboinflammation, vascular dysfunction, and disease progression in COVID-19. Platelet activation triggers the release of inflammatory mediators and promotes platelet-leukocyte interactions, amplifying the systemic inflammatory response and exacerbating endothelial injury. Additionally, platelet-derived factors contribute to microvascular thrombosis, further exacerbating tissue damage and organ dysfunction in severe COVID-19. Elevated sP-selectin levels serve as biomarkers for disease severity and prognostication, aiding in risk stratification and early identification of patients at higher risk of adverse outcomes. Therapeutic strategies targeting platelet dysfunction and sP-selectin-mediated pathways hold promise in mitigating thromboinflammation and improving outcomes in COVID-19 patients. Antiplatelet agents, platelet inhibitors, and anti-inflammatory therapies represent potential interventions to attenuate platelet activation, inhibit platelet-leukocyte interactions, and alleviate endothelial dysfunction. A comprehensive understanding of the multifaceted connection between platelets, sP-selectin, and COVID-19 pathogenesis offers opportunities for tailored therapeutic approaches aimed at mitigating thromboinflammation and improving patient outcomes in this complex and challenging clinical setting.
Identifiants
pubmed: 39118706
doi: 10.1097/MS9.0000000000002302
pii: AMSU-D-24-00732
pmc: PMC11305715
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
4634-4642Informations de copyright
Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc.
Déclaration de conflit d'intérêts
The authors declare no conflicts of interest.