Deficiency of NOX1 or NOX4 Prevents Liver Inflammation and Fibrosis in Mice through Inhibition of Hepatic Stellate Cell Activation.

Searching for effective Smad3 gene-based gene therapies for hepatic fibrosis, we constructed siRNA expression plasmids targeting the rat Smad3 gene and then delivered these

Role of NOX4 in Liver Fibrosis.. pathogenesis of this disease. From these studies, several key generalizations have been done [1]: i) TGF- b is the most potent liver

The presence of viable or non-viable eggs failed to diminish a large induction (10–14-fold) of CTGF expression ( p < 0.01) by treatment with TGF- b by 24 h, but by 72 h this

Gene transfer strategies include inhibition of pro-inflammatory cytokines, blockade of cartilage-de- grading metalloproteinases, inhibition of synovial cell activation and

Inhibition of allergic airway inflammation in mice lacking nitric oxide synthase 2. Role of exhaled nitric oxide

Their shared other ligand CCL5 is known to be involved in this process, as CCL5 2 / 2 mice also showed lower degree of experimental liver fibrosis associated with reduced stellate

The results demonstrated that activation of PP2Ca by overexpression or the new discovered small molecular activator NPLC0393 terminated TGFb-Smad3 and TGFb-p38 signaling

Our recent studies in methionine and choline deficient (MCD) diet fed mice, which develop hepatic steatosis, inflammation, apoptosis, and fibrosis histologically similar to human