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
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

4634-4642

Informations 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.

Auteurs

Emmanuel Ifeanyi Obeagu (EI)

Department of Medical Laboratory Science, Kampala International University.

Getrude Uzoma Obeagu (GU)

School of Nursing Science, Kampala International University.

Patrick Maduabuchi Aja (PM)

Department of Biochemistry, Faculty of Biomedical Sciences, Kampala International University, Ishaka, Uganda.
Department of Biochemistry, Faculty of Sciences, Ebonyi State University, Ebonyi State.

G I A Okoroiwu (GIA)

Department of Nursing Sciences, Faculty of Allied Health Sciences, Bayero University, Kano, Kano State.

N I Ubosi (NI)

Department of Nursing Sciences, Faculty of Allied Health Sciences, Bayero University, Kano, Kano State.

Theophilus Pius (T)

Department of Medical Laboratory Science, Kampala International University.

Muhammad Ashiru (M)

Department of Nursing Sciences, Faculty of Allied Health Sciences, Bayero University, Kano, Kano State.

Kingsley Akaba (K)

Department of Haematology, University of Calabar, Calabar, Cross-River State.

Teddy Charles Adias (TC)

Department of Haematology and Blood Transfusion Science, Faculty of Medical Laboratory Science, Federal University Otuoke, Bayelsa State, Nigeria.

Classifications MeSH