Silencing of PKG1 Gene Mimics Effect of Aging and Sensitizes Rat Vascular Smooth Muscle Cells to Cardiotonic Steroids: Impact on Fibrosis and Salt Sensitivity.
melatonin ameliorated diabetic myocardial ischemia-reperfusion injury through cGMP-PKGIalpha by modulating Nrf-2-HO-1 and MAPK signaling thus reducing myocardial apoptosis and oxidative stress and preserving cardiac function
Our results demonstrate PKG-Ialpha might play an important role in the protective effects of scutellarin on endothelial dysfunction against myocardial ischemic reperfusion injury.
Tumor cell implantation into the tibia induced upregulation of cGKI messenger ribonucleic acid and protein in dorsal root ganglia and hyperexcitability in DRG neurons. Continuing activation of this pathway is needed for hyperalgesia and/or allodynia.
evidence that in podocytes protein kinase G type I a modulates the insulin signaling pathway and glucose transport and that podocyte resistance to the actions of insulin on glucose transport could contribute to the pathogenesis of diabetic podocytopathy
PKG positively regulates proteasome activities and proteasome-mediated degradation of misfolded proteins likely through posttranslational modifications to proteasome subunits.
Hydrogen peroxide may enhance the activity of cGMP-dependent protein kinase type Ialpha (PKG Ialpha) dependent vasodilatation via increased dimerization of the enzyme.
Spironolactone lowers portal hypertension by improvement of liver fibrosis and inhibition of intrahepatic vasoconstriction via down-regulating ROCK-2 activity and activating NO/PKG pathway
elevated cGMP produced either by the guanylate cyclase activator SNAP or the guanylate cyclase activator BNP exerts cytoprotective effects via a common downstream signaling pathway involving PKG activation
increased expressions of PKG I and StAR complex accompanied by decreased PDE5 activity suggest that NO-cGMP signalling pathway and consequent activation of StAR protein regulate the adaptive response of Leydig cells to repeated immobilization stress.
NO reduces flow-stimulated O(2)(-) production in thick ascending limbs this occurs primarily via the cGMP/PKG pathway and O(2)(-) scavenging by NO plays a minor role
The results suggest that chronic elevation of cGMP as seen in inflammatory conditions triggers ubiquitination and degradation of PKG-Ialpha in smooth muscle.
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