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Fig. 3 | Cardiovascular Diabetology

Fig. 3

From: MicroRNAs and obesity-induced endothelial dysfunction: key paradigms in molecular therapy

Fig. 3

Obesity, eNOS, miRNAs and endothelial function. Ca2+ activates eNOS which then converts l-Arginine to l-Citrulline, producing NO as a byproduct. NO, synthetized through eNOS phosphorylation in the endothelium, will diffuse to the smooth muscle cells and increase the levels of cGMP, which then induce vasodilatation. During obesity, higher levels of miR-24, miR-155, miR-15b, miR-16, miR-221/222 and miR-765 are expressed and directly inhibit eNOS translation, thereby causing endothelial dysfunction. Other miRNAs have been shown to affect eNOS through indirect signaling pathways such as AKT (miR-21, miR-26, miR-221/222, and miR-486) and Caveolin1 (miR-132 and miR-124). eNOS: endothelial Nitric Oxide Synthase; NO: Nitric Oxide; cGMP: cyclic guanosine monophosphate; Cav1: Caveolin 1; AKT: Protein kinase B

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