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The Role of P-Selectin in COVID-19 Coagulopathy: An Updated Review
Chiara Agrati1, Alessandra Sacchi1, Eleonora Tartaglia1
1National Institute for Infectious Diseases "Lazzaro Spallanzani" I.R.C.C.S., Via Portuense 292, 00146 Rome, Italy.
Insights
Severe COVID-19 involves blood clots and inflammation, disrupting blood vessel interactions. P-selectin plays a key role in this severe disease, potentially serving as a marker and therapeutic target.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Immunology
Background:
- Severe COVID-19 is linked to increased blood clots, cardiovascular issues, and venous thrombotic events.
- The inflammatory response in severe infections disrupts interactions between platelets, endothelium, and leukocytes, leading to COVID-19-associated coagulopathy.
- P-selectin is crucial for endothelial activation, leukocyte recruitment, and migration.
Purpose of the Study:
- To review the role of P-selectin in COVID-19 pathogenesis.
- To explore P-selectin as a potential severity marker for COVID-19.
- To discuss P-selectin as a target for therapeutic interventions.
Main Methods:
- Literature review and synthesis of current knowledge on P-selectin.
- Analysis of P-selectin's involvement in endothelial activation and leukocyte interactions.
- Evaluation of P-selectin's potential as a biomarker and therapeutic target.
Main Results:
- P-selectin is expressed on activated platelets and endothelial cells during severe COVID-19.
- P-selectin mediates key processes contributing to COVID-19-associated coagulopathy.
- Evidence suggests P-selectin's utility as a severity indicator.
Conclusions:
- P-selectin is a significant factor in severe COVID-19 pathogenesis.
- P-selectin may serve as a valuable biomarker for disease severity.
- Targeting P-selectin offers a potential therapeutic strategy for severe COVID-19.
Abstract:
In severe COVID-19, which is characterized by blood clots and neutrophil-platelet aggregates in the circulating blood and different tissues, an increased incidence of cardiovascular complications and venous thrombotic events has been reported. The inflammatory storm that characterizes severe infections may act as a driver capable of profoundly disrupting the complex interplay between platelets, endothelium, and leukocytes, thus contributing to the definition of COVID-19-associated coagulopathy. In this frame, P-selectin represents a key molecule expressed on endothelial cells and on activated platelets, and contributes to endothelial activation, leucocyte recruitment, rolling, and tissue migration. Briefly, we describe the current state of knowledge about P-selectin involvement in COVID-19 pathogenesis, its possible use as a severity marker and as a target for host-directed therapeutic intervention.
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