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Of the seven known isoforms, NOX1, NOX2, NOX4 and NOX5 are the most abundantly expressed in kidney cells ( In renal disorders, excessive mitochondrial ROS together with ROS derived from NOX enzymes intensify mitochondrial injury and dissipate the organelle’s membrane potential ( ε amplifies this effect by phosphorylating the organizer subunit p47-phox, thereby further stimulating NOX activity ( + (mt-K_ATP) channels, precipitating a drop in mitochondrial membrane potential ( 2.1.3 Immune-cell-derived ROS in sepsis-associated AKI Sepsis is the leading cause of acute kidney injury (AKI) in the intensive-care setting, responsible for roughly 40–50% of all episodes and markedly raising in-hospital mortality risk ( − ) and hypochlorous acid (HOCl) to kill microbes ( − into highly bactericidal hypochlorous acid ( − per million cells per minute during the oxidative burst ( − and inducing oxidative stress ( − ( − , which leads to protein nitration in renal tubules and directly damages tubular cells ( − is a potent oxidant, with greater toxicity than NO, and is involved in endothelial dysfunction ( phox /NOX2-deficient mice, suggesting that myeloid cell-mediated, NOX2-dependent oxidative burst may contribute to the establishment of the renal oxidative microenvironment in AKI and thereby promote tissue injury progression (65)
