We appreciate the insightful comments by Richardson E et al. [1] about our letter [2], which contributed to better explore the fundamental concepts of our study by providing important, additional information for reflection. The identification of additional mechanisms involved in the endothelial damage as that described by Richardson et al. [1] mediated by the p38 MAPK pathway, which is upregulated as a result of the binding of SARSCoV2 on ACE2 receptors on the surface of endothelial cells and, in turn, activates the transcription of the proinflammatory cytokines.

Defibrotide in the COVID-19 coagulopathy: what is the timing?

Macciò, Antonio;Madeddu, Clelia;Caocci, Giovanni;La Nasa, Giorgio
2020-01-01

Abstract

We appreciate the insightful comments by Richardson E et al. [1] about our letter [2], which contributed to better explore the fundamental concepts of our study by providing important, additional information for reflection. The identification of additional mechanisms involved in the endothelial damage as that described by Richardson et al. [1] mediated by the p38 MAPK pathway, which is upregulated as a result of the binding of SARSCoV2 on ACE2 receptors on the surface of endothelial cells and, in turn, activates the transcription of the proinflammatory cytokines.
2020
Coagulopathy; COVID-19; Defibrotide; Resistance; Tolerance
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11584/296502
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