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Endothelial injury generated directly by intracellular viral replication and by ACE2 downregulation, exposing cells to angiotensin II in the absence of the modulator effects of angiotensin 17 (Vinciguerra et al., 2020), and vascular chronic inflammation promoting the development of tissue macrophages overloaded by cholesterol (foam cells), both increase the possibility of acquiring a severe COVID-19 infection (Vinciguerra et al., 2020

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