Nuclear factor erythroid 2-related factor 2 (Nrf2) (Nrf2)

"Antioxidant pathway activation" is not a specific molecule or receptor but refers to the upregulation of cellular defense mechanisms against oxidative stress. The most canonical molecular target associated with this concept is **Nuclear factor erythroid 2-related factor 2 (Nrf2)**. Nrf2 is a transcription factor that regulates the expression of numerous antioxidant and cytoprotective genes by binding to the antioxidant response element (ARE) in their promoters. Under basal conditions, Nrf2 is sequestered in the cytoplasm by its inhibitor Keap1 and targeted for degradation. Upon oxidative stress or exposure to certain drugs/compounds, Nrf2 dissociates from Keap1, translocates into the nucleus, and activates genes involved in detoxification and antioxidative defense such as glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT), NAD(P)H quinone oxidoreductase 1 (NQO1), heme oxygenase‑1 (HO‑1), among others[3][8]. Activation of this pathway plays critical roles in protecting cells from oxidative damage implicated in diseases like cancer, neurodegeneration, cardiovascular disorders, and inflammation[3][4]. However, persistent activation can contribute to tumor progression by enhancing cell survival and drug resistance mechanisms[2]. **Note:** "Antioxidant pathway activation" itself is not a single molecular target but rather describes an effect mediated primarily through targets like **Nrf2**; thus it should be mapped specifically to "Nuclear factor erythroid 2-related factor 2" for structured data purposes.

Other names

NFE2L2Nrf-2nuclear factor (erythroid-derived 2)-like 2Antioxidant response pathway (as a process)Keap1-Nrf2-ARE pathway

Activation of antioxidant gene transcription via ARE binding after release from Keap1 inhibition[3][8]