Cell death is a fundamental process in both physiological and pathological contexts. Unlike classical apoptotic or necrotic cell death, ferroptosis is defined by a unique dependence on iron-catalyzed lipid peroxidation. Its discovery and characterization have provided new insights into lipid metabolism, redox biology, and the role of iron in cellular homeostasis. The core mechanism of ferroptosis involves the failure of antioxidant defense systems to prevent oxidative damage, leading to uncontrolled lipid peroxidation and eventually causing membrane rupture and cell death. NADPH oxidases (NOX), which generate reactive oxygen species (ROS) at cellular membranes, play a significant role in driving the oxidative stress that triggers and propagates ferroptosis. Understanding how NOX enzymes influence ferroptosis may reveal novel strategies to combat diseases caused by excessive activation of these enzymes.

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Ferroptosis and NADPH Oxidases

  • Shaojie Cui,
  • Jin Ye

摘要

Cell death is a fundamental process in both physiological and pathological contexts. Unlike classical apoptotic or necrotic cell death, ferroptosis is defined by a unique dependence on iron-catalyzed lipid peroxidation. Its discovery and characterization have provided new insights into lipid metabolism, redox biology, and the role of iron in cellular homeostasis. The core mechanism of ferroptosis involves the failure of antioxidant defense systems to prevent oxidative damage, leading to uncontrolled lipid peroxidation and eventually causing membrane rupture and cell death. NADPH oxidases (NOX), which generate reactive oxygen species (ROS) at cellular membranes, play a significant role in driving the oxidative stress that triggers and propagates ferroptosis. Understanding how NOX enzymes influence ferroptosis may reveal novel strategies to combat diseases caused by excessive activation of these enzymes.