Tubular NOX4 expression decreases in chronic kidney disease but does not modify fibrosis evolution.

Background: NADPH oxidase 4 (NOX4) catalyzes the formation of hydrogen peroxide (HO). NOX4 is highly expressed in the kidney, but its role in renal injury is unclear and may depend on its specific tissue localization.

Methods: We performed immunostaining with a specific anti-NOX4 antibody and measured NOX4 mRNA expression in human renal biopsies encompassing diverse renal diseases.

Selective pharmacological inhibition of DDR1 prevents experimentally-induced glomerulonephritis in prevention and therapeutic regime.

Background: Discoidin domain receptor 1 (DDR1) is a collagen-activated receptor tyrosine kinase extensively implicated in diseases such as cancer, atherosclerosis and fibrosis. Multiple preclinical studies, performed using either a gene deletion or a gene silencing approaches, have shown this receptor being a major driver target of fibrosis and glomerulosclerosis.

Methods: The present study investigated the role and relevance of DDR1 in human crescentic glomerulonephritis (GN).

Tubular Cytoplasmic Expression of Zinc Finger Protein SNAI1 in Renal Transplant Biopsies: A Sign of Diseased Epithelial Phenotype?

The aim of the present study was to analyze in vivo the role of zinc finger protein SNAI1 (SNAI1) on renal fibrosis. Unilateral ureteral obstruction injury was induced in Snai1 knockout mice. Snai1 gene deletion was, however, only partial and could therefore not be correlated to reduced fibrosis.

NOX1 is responsible for cell death through STAT3 activation in hyperoxia and is associated with the pathogenesis of acute respiratory distress syndrome.

Reactive oxygen species (ROS) contribute to alveolar cell death in acute respiratory distress syndrome (ARDS) and we previously demonstrated that NOX1-derived ROS contributed to hyperoxia-induced alveolar cell death in mice. The study investigates whether NOX1 expression is modulated in epithelial cells concomitantly to cell death and associated to STAT3 signaling in the exudative phase of ARDS. In addition, the role of STAT3 activation in NOX1-dependent epithelial cell death was confirmed by using a lung epithelial cell line and in mice exposed to hyperoxia.