TNF and endothelial dysfunction: The combined effects of RAAS activation, IR, hemodynamic changes, glomerular filtration impairments, lipotoxicity, and the subsequent inflammatory, adipokine dysfunction, and oxidative stress create a vicious cycle with an overproduction of pro-inflammatory cytokines, pro-fibrotic growth factors, and mediators such as tumor necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta, leptin, and interleukin (IL)-6 favoring endothelial dysfunction and increasing vascular permeability [23,29,32].