NOX1 and endothelial dysfunction: Mechanistically, downregulation of GRK2 in myeloid cells attenuates high-fat diet (HFD)-induced infiltration of macrophages and T lymphocytes into PVAT and lowers the expression of pro-inflammatory mediators such as tumor necrosis factor-α (TNF-α) and NADPH oxidase 1 (Nox1), thereby mitigating endothelial dysfunction [76].