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Under hypoxic conditions, the oxidation of Nt-Cys2 is impaired, stabilizing RGS proteins that then suppress G protein signaling, which is critical for cardiovascular function

The latter is triggered by mediators released from activated leukocytes, such as tumor necrosis factor (TNF), interleukin 1 beta (IL-1) and 6 (IL-6), which induce endothelial cell acquisition of a pro-inflammatory transcriptional program (6, 7)