Together, substantial evidence indicated that altered hepatokine (fetuin-A, SeP, and FGF21), adipokine (leptin, adiponectin, and RBP4), cytokines (IL-6 and TNF-α), EVs (miR-122), and gut-derived factors (SCFAs and TMAO) in NAFLD patients participated in the development of hypertension through inducing inflammation, IR, endothelial dysfunction, and RAAS and SNS activation. Here, LEP is linked to endothelial dysfunction.