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Thrombotic complications of COVID-19 may reflect an upregulation of endothelial tissue factor expression that is contingent on activation of endosomal NADPH oxidase

Mechanistically, PRPS1 serine 83 (S83) and threonine 166 (T166) O -GlcNAcylation mediated by OGT leads to PRPS1 hexamer formation and reduction of feedback inhibition of PRPS1 activity, thereby promoting PRPS1 activation, nucleotide synthesis and NAD production

As a result, glutathione remains ineffective as it is not enough to fight off oxidative stress

Overexpression of these mi-RNAs increased ECM degradation, the inflammatory response, and MMP-13 expression in chondrocytes