Nox1, a member of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family, is crucial for generating reactive oxygen species (ROS) [2,4,5]. It participates in various signaling pathways, such as those related to cell migration, proliferation, and inflammation [4]. Its activity is regulated at transcriptional and post-translational levels, and it is activated in response to different agonists [4]. Genetic models, like Nox1-deficient mice, have been instrumental in understanding its functions.

In IBD, Nox1-deficient murine colonoids showed lower TNFα-induced ROS production compared to wild-type ones. Also, Nox1-deficient colonoids had abnormal M cell induction, with enhanced basal lymphoplasmacytosis, suggesting Nox1's role in maintaining stem cell niche and cell differentiation in the intestine [1]. In cardiovascular diseases, Nox1-knockout in smooth muscle cells reduced abdominal aortic aneurysm formation, accompanied by decreased ROS, monocyte/macrophage infiltration, and elastin fragmentation, indicating its role in vascular inflammation and extracellular matrix remodeling [6]. In repetitive behavior studies, Nox1-deficient mice had inhibited compulsive-like repetitive behaviors, and Nox1 was involved in D2 receptor-mediated synaptic potentiation in the striatum [3].

In conclusion, Nox1 is essential for ROS-related functions in multiple biological processes. Gene knockout mouse models have revealed its significance in diseases such as IBD, cardiovascular diseases, and those related to repetitive behaviors. Understanding Nox1's functions provides potential therapeutic targets for these diseases.