NOX4 (NADPH Oxidase 4)

Compared to normal tissue an increased expression of NOX4, OGG1, MSH2/MSH6 proteins and phospho-Smad3 was found in RAI Refractory BRAFV600E mutated tumors. Collectively, our findings reveal a mechanistic basis for NOX4's role in thyroid dedifferentiation.

This study demonstrates that the anti-pigmentation effect of NnE and its bioactive compound, quercetin 3-O-glucuronide, is mediated through the YAP-ATG5 signaling axis and Q3Q-driven NOX4 inhibition, which establishes the mechanistic basis for their potential application in preventing UVB-induced skin pigmentation and provides a novel perspective for the development of anti-photoaging interventions.

However, those in silico predictions require experimental validation. This work provides the first computational evidence of potential lipopeptide-receptor interactions and establishes a foundation for future experimental investigation of probiotic-derived therapeutics.

TAC-induced vascular dysfunction seen in breast cancer survivors is absent in premenopausal women, likely owing to estrogen-mediated protection against oxidative stress and eNOS inhibition.

HHSY effectively treats liver fibrosis, likely by inhibiting HSC activation through the NOX4/ROS/NLRP3 pathway. This underscores HHSY's clinical relevance as a potential therapeutic option for liver fibrosis.

Moreover, ER stress inducer thapsigargin (TG) mediates synergistic apoptotic cell death in CBD-treated HCT116 and HT29 cells...We established radioresistant CRC models (HCT116R and HT29R); subsequently, radiation (2 Gy) in combination with CBD treatment overcame radioresistance via the modulation of the epithelial-mesenchymal transition (EMT) phenomenon, including the increase in N-cadherin and vimentin and the reduction in E-cadherin. Thus, these results show that CBD may be a new powerful therapeutic approach for CRC radiotherapy.

These results demonstrate that F-9 cancer cells are significantly more sensitive to SELENOV than normal fibroblasts, with 50 µg/mL sufficient to trigger mitochondrial dysfunction, oxidative stress, and apoptosis. The findings highlight SELENOV's potential as a targeted anticancer agent, particularly for germ cell tumors.

A systematic framework implementing machine-learning approaches and AUcell analysis was established for identifying core ferroptosis genes and validating their functional link to ferroptosis. Meanwhile, a reliable ferroptosis-associated signature was established, which shed new light on the ferroptosis-mediated molecular mechanisms and therapeutic potential underlying CRC.

Colon cancer patients with upregulated NOX4, CXCL8, CXCL5, GDF15, or MMP13 may not benefit from aspirin chemoprophylaxis. Conversely, patients showing aspirin-induced downregulation of E2F1, CCNE1, VEGFA, and MMP3 may derive chemoprophylactic benefit.

Similarly, EGCG treatment in X-irradiated BV2 cells reduced TLR4, NOX3, and NOX4 expression, decreased cytosolic Nrf2 levels while upregulating nuclear Nrf2 expression, and enhanced HO-1 expression, leading to a reduction in ROS production. These findings suggest that EGCG may be a promising therapeutic strategy to restore X-irradiation-induced damage in the central nervous system, promoting hippocampal neurogenesis, memory function, and synapse development.

Histological changes, transforming growth factor-β (TGF-β) immuno-expression were also evaluated. CZ caused a significant reduction in placental oxidative stress, inflammation and apoptosis induced by CP. Current study revealed that CZ protective role against CP-induced placental damage involves modulation of TGF-β/NOX4 signaling pathway (Fig. 1). Fig. 1 Graphical abstract of our manuscript.

Overall, this study confirmed that LYMS is an independent prognostic risk factor in GC patients. The LYMS demonstrates significant predictive ability for responses to immunotherapy, suggesting its potential to guide future immunotherapy interventions for GC patients.