Journal: Viruses
Article Title: Impact of SARS-CoV-2 Wuhan and Omicron Variant Proteins on Type I Interferon Response
doi: 10.3390/v17040569
Figure Lengend Snippet: Mechanisms of endothelial dysfunction in COVID-19. The figure illustrates the key mechanisms driving endothelial dysfunction in COVID-19 and their downstream effects on the vascular system that can lead to fatal organ damage. ( A ) Direct SARS-CoV-2 infection: The viral spike protein binds to ACE2 receptors expressed on endothelial cells, facilitating viral entry and replication, leading to cellular damage [ , , ]. ( B ) Systemic inflammation: Elevated pro-inflammatory cytokines, including IL-6, IL-1β, and TNF-α, activate endothelial cells, inducing an amplified inflammatory response [ , , , ]. ( C ) Hypercoagulable state: Endothelial injury promotes thrombin generation and platelet aggregation, resulting in the formation of thrombi and widespread vascular occlusion [ , ]. ( D ) Hypoxia: Reduced oxygen delivery due to severe respiratory distress exacerbates endothelial dysfunction, further impairing tissue oxygenation [ , ]. ( E ) Complement activation: Overactivation of the complement cascade causes endothelial damage and contributes to pro-thrombotic states through the generation of C3 and C5 convertases [ , , ].
Article Snippet: They were cultured in Human Large Vessel Endothelial Cell Basal Medium (formerly Medium 200) (Thermo Fisher Scientific) supplemented with Large Vessel Endothelial Supplement (LVES) (Thermo Fisher Scientific), 2 mM L-glutamine (Thermo Fisher Scientific), and 100 U/mL penicillin and 100 μg/mL streptomycin (Thermo Fisher Scientific).
Techniques: Infection, Amplification, Activation Assay