Figure 2.

Biological role of NO in pathophysiological conditions. NO-mediated activation of cGMP, PKG, and VASP can cause platelet inhibition while NO-mediated induction of pro-apoptotic proteins such as PARP, AIF, cytochrome C, and cleaved caspase-3 can induce cell death. NO-mediated activation of cGMP, PKG, Rho A, and Rho kinase can alter smooth muscles relaxation. Inhibition of NAD, NADPH, and GSH by NO increases the probability of cell death. Lipid peroxidation caused by NO induces oxidative stress or damage. S-nitrosylation elicited by NO can cause neurotoxicity or neurodegeneration. NO-mediated induction of PKG and calcium signaling causes exitotoxicity and contraction effects. NO is also involved in neutrophil infiltration and endothelial dysfunctions through effects of mitochondrial respiration, through NK cell toxicity, and through activation of the GAPDH-PARP pathway and its functions.