This leads to increased oxidative stress levels, affects endoplasmic reticulum (ER) homeostasis, activates ER stress (ERS) (Lindholm et al., 2017), and mediates high expression of inflammatory factors such as NF-κB, TNF-α, matrix metalloproteinases, causing endothelial dysfunction, collagen fiber proliferation, and smooth muscle cell apoptosis. Here, TNF is linked to endothelial dysfunction.