Figure 1

Figure 1. NO in pathophysiological conditions. NO-mediated activation of cGMP, PKG, and VASP can cause platelet inhibition, whereas NO-mediated induction of pro-apoptotic proteins (PARP, AIF, cytochrome C, and cleaved caspase-3) can induce cell death. Furthermore, NO-mediated activation of cGMP, PKG, Rho A, and Rho kinase can alter smooth muscle relaxation, whereas inhibition of NAD, NADPH, and GSH by NO increases cell death. Moreover, lipid peroxidation caused by NO leads to oxidative stress or damage, and S-nitrosylation induced by NO may lead to neurotoxicity or neurodegeneration. In addition, NO-mediated induction of PKG and calcium signaling leads to excitotoxicity and contraction effects. NO is also involved in neutrophil infiltration and endothelial dysfunction through effects on mitochondrial respiration, NK cell toxicity, and activation of the GAPDH-PARP pathway and its functions [26].