Fig. 4
From: MicroRNAs and obesity-induced endothelial dysfunction: key paradigms in molecular therapy
Obesity, SIRT1, miRNAs and endothelial function. SIRT1 directly deacetylates eNOS, PGC-1 α, p53, and FoxO1 leading to enhanced NO bioavailability and mitochondrial biogenesis as well as, decreased senescence, angiogenesis, apoptosis, and oxidative stress. All of these effects allow for the maintenance of endothelial homeostasis. Levels of miRNAs that directly target SIRT1 and thereby modulate endothelial function can be either increased (miR-204, miR-34a, miR-132, miR-217 and miR-200c) or decreased (miR-149) in obesity. SIRT1: Sirtuin 1; eNOS: endothelial Nitric Oxide Synthase; NO: Nitric Oxide; ROS: Reactive oxygen species; SOD2: Superoxide dismutase; P53: Tumor protein; FoxO: Forkhead box; PGC-1 α: Peroxisome proliferator-activated receptor gamma coactivator 1-alpha