Related studies found that in the aorta of STZ-induced diabetic ApoE−/− mice, the levels of NOX2 and NOX4 increased; in db/db mice (type II diabetes model), the expression of NOX1 and NOX4 was upregulated, and their activation resulted in the oxidation of ROS downstream molecules (e.g., tetrahydrobiopterin) and increased inflammatory response, indicating that NOX1, NOX2, and NOX4 are all involved in the pathological process of diabetic cardiomyopathy [90]. This evidence concerns the gene NOX1 and diabetic cardiomyopathy.