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.

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