| Source: |
| Type: |
| NOX4 (NADPH oxidase 4) is a member of the NADPH oxidase (NOX) family of enzymes, which are responsible for generating reactive oxygen species (ROS) in various cell types. NOX4 is regulated by hypoxia, which can activate its expression and activity. NOX4 (NADPH oxidase 4) is an enzyme that produces reactive oxygen species (ROS), particularly hydrogen peroxide (H₂O₂). NOX4 is a cytoplasmic enzyme that catalyzes the transfer of electrons from NADPH to oxygen, resulting in the production of superoxide anion (O2-) and other ROS. NOX4 is expressed in a variety of tissues, including the kidney, lung, and vascular smooth muscle cells. NOX4 is generally expressed in cancer. In general, high NOX4 expression is associated with: Poor prognosis Increased tumor size Metastasis Resistance to chemotherapy and radiation therapy Poor response to treatment Low NOX4 expression is associated with: Better prognosis Smaller tumor size Less metastasis Better response to chemotherapy and radiation therapy Better response to treatment The combination of NOX4-driven ROS and available iron can lead to a synergistic increase in oxidative stress, setting the stage for ferroptotic cell death. |
| Normal Healthy |
| 3451- | ALA, | Alpha-lipoic acid ameliorates H2O2-induced human vein endothelial cells injury via suppression of inflammation and oxidative stress |
| - | in-vitro, | Nor, | HUVECs |
| 2724- | BetA, | NOX4_by_betulinic_acid_protects_against_cerebral_ischemia-reperfusion_in_mice">Down-regulation of NOX4 by betulinic acid protects against cerebral ischemia-reperfusion in mice |
| - | in-vivo, | Nor, | NA | - | in-vivo, | Stroke, | NA |
| 2807- | CHr, | Evidence-based mechanistic role of chrysin towards protection of cardiac hypertrophy and fibrosis in rats |
| - | in-vivo, | Nor, | NA |
| 3534- | QC, | Lyco, | Synergistic protection of quercetin and lycopene against oxidative stress via SIRT1-Nox4-ROS axis in HUVEC cells |
| - | in-vitro, | Nor, | HUVECs |
| 3012- | RosA, | Rad, | Rosmarinic Acid Prevents Radiation-Induced Pulmonary Fibrosis Through Attenuation of ROSMYPT1TGFβ1 Signaling Via miR-19b-3p |
| - | in-vitro, | Nor, | IMR90 |
| 966- | RT, | Antioxidant Mechanism of Rutin on Hypoxia-Induced Pulmonary Arterial Cell Proliferation |
| - | vitro+vivo, | Nor, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:49 Cells:% prod#:% Target#:644 State#:% Dir#:1
wNotes=0 sortOrder:rid,rpid