Nox1, a member of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family, is a key enzyme involved in the production of reactive oxygen species (ROS). It participates in multiple cellular processes, including cell signaling, inflammation, and cell migration. Its activity is regulated at transcriptional level, by complex formation, protein stabilization and post-translational modification. Genetic models such as Nox1-deficient mice have been crucial in understanding its role in various biological processes and diseases [2].

In the context of diseases, Nox1-deficiency in mice has shown several effects. In the intestinal epithelium, TNFα-induced ROS secretion was reduced in Nox1-deficient murine colonoids, and there was enhanced induction of M cells, which may contribute to colitis through dysregulation of the stem cell niche [1]. In cardiovascular diseases, Nox1-deficiency in ApoE-/-Nox1SMCko mice (where Nox1 was SMC-specifically deleted) reduced abdominal aortic aneurysm (AAA) formation, decreased abdominal aortic ROS and monocyte/macrophage infiltration, and lessened elastin fragments and matrix metalloproteinase activities [3]. In collagen-induced arthritis, Nox1-KO mice had a lower severity and incidence of the disease following LPS administration [4].

In conclusion, Nox1 plays essential roles in multiple biological processes, especially in ROS-related signaling. The use of Nox1-KO and CKO mouse models has revealed its significant contributions to diseases such as colitis, cardiovascular diseases, and arthritis. Understanding Nox1 function provides potential therapeutic targets for these diseases.