KEAP1 (Kelch Like ECH Associated Protein 1)

Beyond oncology, TRIM16 protects against neurodegenerative, cardiovascular, and inflammatory diseases through quality control mechanisms. This review integrates recent advances to elucidate TRIM16's molecular mechanisms and disease-specific functions, emphasizing its therapeutic and biomarker potential, and outlines future directions to decode its context-dependent actions for clinical translation.

This review provides a comprehensive synthesis of the sources, pharmacological actions, safety, pharmacokinetics, and potential applications of GS. Future research should focus on structural modification of GS, development of novel formulations, and exploration of synergistic combinations with other therapeutic agents to broaden its clinical utility.

Together, these findings provide the first molecular evidence that PFHxS acts as an environmental driver of GC progression by targeting KEAP1, while also delivering a clinically relevant prognostic tool. This work highlights a previously unrecognized environmental risk factor for gastric cancer and offers new perspectives for risk assessment, prevention, and therapeutic intervention.

Astraflavonol H increased NRF2 protein stability and attenuated tumor necrosis factor-α-induced Janus-activated kinase and signal transducer and activator of transcription-1 phosphorylation. Overall, this study highlights the potential of A. membranaceus sprouts and their components as anti-aging foods.

In summary, our mechanistic investigations revealed TFAP2C as a novel oncogenic driver in OC and a key regulator of ferroptosis via its epigenetic modulation of the KEAP1-NRF2 axis. These findings highlight TFAP2C as a potential therapeutic target for ferroptosis-inducing therapies in OC patients with high TFAP2C expression.

TTF-1 negativity identifies a subset of LUAD with worse outcomes to immunotherapy, chemo-immunotherapy, and KRASG12C inhibitors.

HO-1 showed a significant inverse correlation with HMGB-1 (r = -0.405, p = 0.001), KEAP1 was positively correlated with sST2 (r = 0.282, p = 0.029), and GPX4 was correlated with FGF21 (r = 0.255, p = 0.049); no other significant associations were found. β-thalassemia major patients exhibit significant endothelial and cardiac injury markers, altered lipid profiles, and selective upregulation of antioxidant and ferroptosis-related genes.

Bioavailability, microbiota-driven biotransformation, and dose realism are considered the primary determinants of in vivo relevance, rather than secondary or descriptive considerations. Future research should prioritize standardized exposure and metabolite profile, dose-appropriate interventions, harmonized clinical endpoints, and stratification strategies that account for microbiome-driven interindividual variability to improve reproducibility and inform nutraceutical and therapeutic use.

Although dexrazoxane is the only FDA-approved cardioprotective agent, concerns about its long-term safety and potential interference with doxorubicin's antitumor effectiveness have increased the search for safer alternatives. Despite promising preclinical evidence of their antioxidant, anti-inflammatory, and anti-apoptotic properties, the clinical use of phytochemicals is limited by issues such as low bioavailability, poor specificity, dose-dependent toxicity, variable pharmacokinetics, and lack of standardisation. Therefore, innovative approaches-such as ligand-targeted delivery systems, nanotechnology-based formulations, and structural modifications of lead compounds-are essential to enhance their pharmacological properties, safety, and therapeutic effectiveness for effective cardioprotection against doxorubicin-induced toxicity.

In an orthotopic 4T1 model, FCA-PDT-RT achieved superior tumor control at only 12 Gy, which correlated with increased CD3+/CD8+ T cell infiltration and suppressed angiogenesis, while maintaining favorable safety. FCA thus enables synergistic PDT-RT through sequential microenvironment remodeling, oxidative amplification, and metabolic exhaustion, offering a dose-sparing strategy with translational promise for breast cancer therapy.

Therefore, it might be indicated that BT improved Dox retention and increased the Dox responsiveness in A549 cells. BT-mediated selective suppression of the NRF2, re-stabilized the KEAP-1-independent NRF2 regulators and made the non-responsive A549 cells partially sensitive to Dox.

In addition to inhibiting LPS-induced macrophage activation, DC activates the Nrf2 signaling pathway in hepatocytes to alleviate inflammation-enhanced liver ferroptosis. It provides potential therapeutic strategies for sepsis and Gram-negative bacteria-associated liver injury.