NQO1, also known as NAD(P)H: quinone oxidoreductase 1, is an antioxidant enzyme. It uses NADH or NADPH as substrates to reduce quinones to hydroquinones, protecting cells from oxidative stress. NQO1 is involved in multiple cellular processes such as redox control, and its functions include superoxide reductase activity, NAD+ generation, and protein stabilization [1]. It is also associated with pathways like TLR4/NF-κB and TGF-β/Smad, and is of great biological importance in various physiological and pathological conditions [2].

In diabetic nephropathy, NQO1 alleviates renal fibrosis. Overexpression of NQO1 in the kidneys of db/db mice and HG-cultured HK-2 cells suppressed inflammation, extracellular matrix accumulation, and epithelial-mesenchymal transition by inhibiting the TLR4/NF-κB and TGF-β/Smad signaling pathways [2]. In drug-resistant non-small cell lung cancer, the NQO1 substrate MAM induced ferroptosis, and this effect was abolished by NQO1 inhibitor, siRNA, etc. [3]. In CNS disorders, impairment of NQO1 activity is linked to multiple neurological disorders, and its dysregulation may contribute to the pathophysiological mechanisms [4]. In ovarian cancer, NQO1 is reported to have an impact on the onset and progression of the disease [5].

In conclusion, NQO1 plays essential roles in protecting cells from oxidative stress and is involved in various disease-related processes such as fibrosis in diabetic nephropathy, ferroptosis in drug-resistant lung cancer, and neurological disorders. The study of NQO1 through in vivo models like db/db mice helps to understand its functions in specific disease conditions, providing potential targets for disease treatment and prevention.