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Updated: Oct 8, 2025

Author Spotlight: A Novel Method for Comprehensive Cell Component Analysis of Cerebral Blood Clots
Published on: July 21, 2023
Fundamentals in Covid-19-Associated Thrombosis: Molecular and Cellular Aspects
Daniella M Mizurini1, Eugenio D Hottz2,3, Patrícia T Bozza2
1Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro (UFRJ), Rio de Janeiro, Brazil.
Insights
COVID-19 (coronavirus disease) is linked to blood clots due to inflammation and cellular activation. This review explores the cellular mechanisms behind COVID-19-associated thrombosis, impacting patient outcomes.
Area of Science:
- Hematology
- Infectious Diseases
- Pathophysiology
Background:
- COVID-19 (coronavirus disease) presents a high risk of coagulopathy and venous thromboembolism.
- Elevated D-dimer levels are a common laboratory finding in severe COVID-19 cases.
- SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus-2) infection triggers a cytokine storm, activating vascular cells.
Purpose of the Study:
- To review the cellular mechanisms contributing to thrombosis in COVID-19 patients.
- To elucidate the complex interplay of factors leading to a prothrombotic state.
Main Methods:
- Literature review of studies on COVID-19, thrombosis, and coagulation.
- Analysis of proposed cellular and molecular pathways involved in COVID-19-associated coagulopathy.
Main Results:
- COVID-19-associated thrombosis involves a complex interaction between vascular cells (endothelial cells, platelets, monocytes, neutrophils) and soluble plasma factors.
- Pro-inflammatory cytokines play a key role in activating these cellular components.
- The coagulation cascade and complement system are implicated in the prothrombotic state.
Conclusions:
- Understanding the cellular mechanisms of COVID-19-associated thrombosis is crucial for managing patient outcomes.
- Targeting these cellular pathways may offer therapeutic strategies for preventing or treating thromboembolism in COVID-19.
Abstract:
The novel coronavirus disease (COVID-19) is associated with a high incidence of coagulopathy and venous thromboembolism that may contribute to the worsening of the clinical outcome in affected patients. Marked increased D-dimer levels are the most common laboratory finding and have been repeatedly reported in critically ill COVID-19 patients. The infection caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) is followed by a massive release of pro-inflammatory cytokines, which mediate the activation of endothelial cells, platelets, monocytes, and neutrophils in the vasculature. In this context, COVID-19-associated thrombosis is a complex process that seems to engage vascular cells along with soluble plasma factors, including the coagulation cascade, and complement system that contribute to the establishment of the prothrombotic state. In this review, we summarize the main findings concerning the cellular mechanisms proposed for the establishment of COVID-19-associated thrombosis.
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