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Tissue factor in COVID-19-associated coagulopathy.
Subramaniam, Saravanan; Kothari, Hema; Bosmann, Markus.
  • Subramaniam S; Pulmonary Center, Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA. Electronic address: ssubra@bu.edu.
  • Kothari H; Carter Immunology Center, University of Virginia, Charlottesville, VA 22908, USA; Cardiovascular Division, Department of Medicine, University of Virginia, Charlottesville, VA 22908, USA.
  • Bosmann M; Pulmonary Center, Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA; Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.
Thromb Res ; 220: 35-47, 2022 12.
Article in English | MEDLINE | ID: covidwho-2106047
ABSTRACT
Evidence of micro- and macro-thrombi in the arteries and veins of critically ill COVID-19 patients and in autopsies highlight the occurrence of COVID-19-associated coagulopathy (CAC). Clinical findings of critically ill COVID-19 patients point to various mechanisms for CAC; however, the definitive underlying cause is unclear. Multiple factors may contribute to the prothrombotic state in patients with COVID-19. Aberrant expression of tissue factor (TF), an initiator of the extrinsic coagulation pathway, leads to thrombotic complications during injury, inflammation, and infections. Clinical evidence suggests that TF-dependent coagulation activation likely plays a role in CAC. Multiple factors could trigger abnormal TF expression and coagulation activation in patients with severe COVID-19 infection. Proinflammatory cytokines that are highly elevated in COVID-19 (IL-1ß, IL-6 and TNF-α) are known induce TF expression on leukocytes (e.g. monocytes, macrophages) and non-immune cells (e.g. endothelium, epithelium) in other conditions. Antiphospholipid antibodies, TF-positive extracellular vesicles, pattern recognition receptor (PRR) pathways and complement activation are all candidate factors that could trigger TF-dependent procoagulant activity. In addition, coagulation factors, such as thrombin, may further potentiate the induction of TF via protease-activated receptors on cells. In this systematic review, with other viral infections, we discuss potential mechanisms and cell-type-specific expressions of TF during SARS-CoV-2 infection and its role in the development of CAC.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Thrombosis / Blood Coagulation Disorders / COVID-19 Type of study: Prognostic study / Reviews / Systematic review/Meta Analysis Topics: Long Covid Limits: Humans Language: English Journal: Thromb Res Year: 2022 Document Type: Article

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Thrombosis / Blood Coagulation Disorders / COVID-19 Type of study: Prognostic study / Reviews / Systematic review/Meta Analysis Topics: Long Covid Limits: Humans Language: English Journal: Thromb Res Year: 2022 Document Type: Article