Aquaporin Membrane Channels in Oxidative Stress, Cell Signaling, and Aging: Recent Advances and Research Trends

Figure 1

NO release by eNOS in physiological and peroxidative conditions. While “coupled” eNOS is involved in the physiological NO release underlying vasorelaxation, NO release by “uncoupled” eNOS is turned into OONO⁻ (peroxynitrites) leading to an increase in oxidative stress with consequent endothelial dysfunction. ADMA: asymmetric dimethylarginine; Akt: protein kinase B; BH4: tetrahydrobiopterin; CAM: calmodulin; Cav-1: caveolin 1; eNOS: endothelial NO synthase; cGMP: cyclic guanosine monophosphate; GTP: guanosine triphosphate; GTPCH: guanosine triphosphate cyclohydrolase I; Hsp 90: heat shock protein 90; NADPH: nicotinamide adenine dinucleotide phosphate; NO: nitric oxide; sGC: soluble guanylate cyclase; PKG: protein kinase G.