NOX1 (NADPH oxidase 1) is an X-linked enzyme that catalyzes superoxide generation from molecular oxygen using NADPH as an electron donor 1. As a key source of reactive oxygen species (ROS), NOX1 functions as both a signaling molecule and a mediator of cellular stress responses across multiple physiological contexts. Mechanistically, NOX1 generates superoxide and hydrogen peroxide that act as secondary messengers in redox-sensitive signaling pathways 2. The enzyme plays critical roles in cell migration, proliferation, and angiogenesis through modulation of integrin biosynthesis and vascular endothelial growth factor production 1. In disease pathology, NOX1 dysregulation contributes to multiple conditions. NOX1 upregulation triggers ferroptosis in Parkinson's disease through activation of ferroptosis-related pathways and ferritinophagy 3. In dilated cardiomyopathy, enhanced NOX1 expression drives NLRP3 inflammasome activation and cardiomyocyte pyroptosis via mitochondrial fission, causing myocardial dysfunction 4. Conversely, NOX1 deficiency impairs intestinal epithelial ROS secretion in inflammatory bowel disease, promoting pathological M cell differentiation and enhanced inflammation through dysregulation of stem cell maintenance pathways 5. Clinically, NOX1/4 inhibition shows therapeutic promise in hepatic fibrosis by reducing oxidative stress and stellate cell activation 6, while NOX1 modulation influences drug sensitivity in retinoblastoma through ferroptosis regulation 7.