IndraLab
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"RLX has been found to inhibit TGF-beta1 signal transduction at the level of intracellular Smad2, either through direct effects on cyclic guanosine monophosphate (cGMP) or by signaling through a RXFP1-extracellular signal regulated kinases (ERK)-1/2 phosphorylation-neuronal nitric oxide (NO) synthase (nNOS)-NO-soluble guanylyl cyclase (sGC)-cGMP-dependent pathway."
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"The use of LY2109761, a selective inhibitor of TGF-beta1 and Smad2, diphenyliodonium (DPI), and/or astragaloside IV (AST IV is a monomer located in an extract of astragaloside) decreased the NOX4 expression, the level of ROS, and the TGF-beta1 and Smad2 expression, suggesting that inhibitions of the NOX4 and TGF-beta1 and Smad2 pathways downregulate apoptosis in HUVECs 30."
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"Additionally, this study provided the first evidence that the NO donor, DEA/NO, could also induce anti-fibrotic actions via a sGC-cGMP-dependent pathway, leading to inhibition of TGF-beta1 signal transduction (at the level of pSmad2) and subsequently, the pro fibrotic influence of TGF-beta1 on renal myofibroblast differentiation, while being able to promote collagen degrading gelatinases (MMP-2 and MMP-9)."