Genomics, phytochemicals, and oxidative stress

This study shows endogenous CGRP activates NRF2 via non-electrophilic mechanisms, with organ-specific pathways and time-dependent effects on oxidative stress resistance.

This study shows that exogenous thyroxine improves antioxidant defenses and reduces oxidative stress in insulin-resistant OLETF rats.

This study identifies TEAD1 as a direct regulator of NRF2 and oxidative stress response in cardiomyocytes, showing its critical role in maintaining antioxidant defenses and its downregulation in heart failure.

This study shows that DDI2 deficiency reduces liver cancer growth by increasing ROS and DNA damage, which inhibits cell survival and tumor progression.

This paper identifies Pyrimethamine and its derivative WCDD115 as potent inhibitors of NRF2 by targeting DHFR and one-carbon metabolism, with WCDD115 showing 22-fold greater efficacy.

This study shows hepatic Nrf1 promotes VLDL-dependent liver defense against sepsis by enhancing stress defenses and improving survival.

The paper maps organ-specific electrophile responsivity in C. elegans, identifying proteins that respond to reactive metabolites in a tissue-specific manner.

This study investigates the protective effects of eugenol on type 1 diabetes mellitus by activating the NRF2 pathway, reducing oxidative stress and apoptosis in pancreatic β cells.

This study shows Nrf2 modulates CD4+ T-cell activation and expansion by altering glucose and glutamine metabolism, offering insights for improving immunotherapies.

This study shows that loss of WDR23 in mice leads to increased NRF2 stability and antioxidant defense, affecting age-related hippocampal behaviors in sex-dependent ways.

This study shows that both acute and chronic diving reflex activate NRF2 signaling, with acute exposure inducing stronger antioxidative gene expression than chronic exposure.

This study shows capsaicin directly binds KEAP1 and allosterically activates NRF2, reducing ethanol-induced gastric oxidative damage and suggesting its potential as a novel NRF2 agonist for oxidative stress-related diseases.

This study shows that transient high glucose exposure induces persistent transcriptional and chromatin changes in endothelial cells, which can be reversed by NRF2 pathway activation.

The paper quantifies Nrf2 expression and chromatin accessibility in CNS single-cell datasets, finding low Nrf2 expression in neurons across species and diseases.

The paper determines the crystal structure of the KEAP1-CUL3 complex and develops a TR-FRET assay to study its binding, showing CDDO reduces affinity without disrupting the interaction.

The paper shows NRF2 activation in KEAP1 wildtype lung cancers causes NADH-reductive stress, making them vulnerable to Complex I inhibition.

This study shows Nrf1 is essential for mitochondrial homeostasis by integrating redox regulatory networks, with loss of Nrf1 leading to increased ROS and oxidative damage.

This study shows that Nrf2 overexpression in cardiomyocytes prevents diabetic cardiomyopathy by reducing oxidative stress and correcting glucose and lipid metabolism.

This study shows that NRF2 regulates thyroglobulin expression in zebrafish and mouse thyroid organoids to manage oxidative stress during thyroid hormone synthesis.

This study identifies SKN-1 as a metabolic surveillance factor that responds to amino acid catabolism to influence stress resistance in C. elegans.

This paper uses mathematical modeling to quantify the signaling properties of the KEAP1-NRF2 system, revealing mechanisms of ultrasensitivity and response dynamics to oxidative stress.

This study shows that NFE2L1 dysfunction leads to AMPK-driven glucose metabolism reprogramming and mitochondrial damage in liver cancer.

This study compares high and low intensity muscle stimulation on Nrf2-mediated redox stress responses in mouse skeletal muscle, finding intensity-dependent activation of Nrf2-ARE binding and downregulation of Keap1.

This study shows PICH, an ATP-dependent chromatin remodeler, co-regulates oxidative stress response with Nrf2 by modulating antioxidant gene expression and interacting with H3K27ac.

The paper identifies synergistic and antagonistic roles of Nfe2l1 and Nfe2l2 in regulating -PalNRF1 and TFAM expression, with species-specific differences observed between mice and humans.

This study discovers the non-transcription factor activity of NFE2L1 in cytoplasm, revealing its tumor suppressive role through Wnt/β-catenin signaling repression, independent of its transcriptional function.

This study identifies Bach2 as a repressor of Nrf2-mediated antioxidant enzyme expression in dopaminergic neurons, explaining limited Nrf2 activity and proposing Bach2 as a drug target for Parkinson's disease.

The paper investigates how different Nrf1 isoforms regulate distinct subsets of target genes, showing that Nrf1{gamma} acts as a dominant-negative competitor to Nrf1/{beta}.

This study shows that Nrf1 knockout leads to Nrf2 hyperactivation, promoting hepatoma, and reveals a feedback loop between Nrf1 and Nrf2 in tumor suppression.

This study investigates the basal role of excess Nrf2 in regulating mRNA and miRNA interactions in the mouse myocardium using transgenic mice and high-throughput sequencing.