Cu2+-chelated epigallocatechin gallate nanoparticle-functionalized hydrogel promotes osteogenesis by inhibiting ferroptosis.

Dual targeting of NCF1 and NLRP3 by roburic acid orchestrates redox homeostasis and inhibits macrophage death in septic lung injury.

14-3-3σ alleviates UVB-induced epidermal oxidative stress through the pentose phosphate pathway promotion.

Mitophagy-activating nanozyme hydrogel for enhanced diabetic wound healing.

Txnrd2 loss in skeletal muscle causes muscle atrophy and drives leanness and obesity resistance.

Enhanced endocrine-metabolic support and axonemal assembly in high-sperm-motility geese: insights from testicular cellular heterogeneity by scRNA-seq.

Host-directed therapy for tuberculosis: Repurposed drugs toward global tuberculosis elimination.

Omics-based molecular signatures of adrenal, kidney, and lung development in male rat offspring exposed to maternal protein restriction.

Systemic crosstalk between liver and brain is associated with microplastic-induced neurobehavioral toxicity in zebrafish.

Hypoxia constitutes a common feature of tumor microenvironments, orchestrating cancer progression across various malignancies. Cancer growth and resistance to therapy are frequently associated with overexpression of antioxidant systems, such as the thioredoxin (Trx) system. This system is fundamental for cell survival and proliferation, playing a key role in maintaining redox homeostasis and regulating hypoxia-inducible factor-1alpha (HIF-1α) activity. This, in turn, regulates different genes involved in tumor progression, such as the vascular endothelial growth factor (VEGF), an indispensable factor for tumor invasiveness and microenvironment tumor maintenance. HIF-1α can also be regulated by the signal transducer and activator of transcription 3 (STAT3), an oncogene stimulated by pro-inflammatory cytokines and growth factors. Targeting antioxidant systems, such as the Trx system, is an emerging strategy in cancer therapy, as tumor cells are more vulnerable to disruptions in redox homeostasis than normal cells. Even though there are some studies correlating the use of Trx inhibitors and the inhibition of hypoxia-related factors, the diverse pathways in which this occurs are still elusive. Therefore, in this review, we explore the multiple pathways through which the Trx system influences HIF-1α and highlight drugs that have been studied targeting hypoxia-related factors by inhibiting the Trx system. Given the link between oxidative stress and apoptosis in cancer cells, and the low overall survival rates for many cancers despite new therapies, understanding the Trx system's connection to hypoxia-related pathways could be crucial for advancing therapeutic approaches and tackling therapy resistance.

α-Ketoglutarate restores redox and energy homeostasis to ameliorate splenic immune dysfunction induced by carbonate-alkaline stress in crucian carp (Carassius auratus).

Arbuscular mycorrhizal consortium alleviates chromium(VI) stress and enhances seed phytochemicals in Psoralea corylifolia L.

Mitochondrial redox homeostasis is essential for cellular metabolism and organismal development. To investigate the consequences of disrupting redox homeostasis in this organelle in a metazoan organism, we generated a double mutant lacking mitochondrial glutathione reductase (gsr-1a) and thioredoxin reductase (trxr-2) genes in Caenorhabditis elegans. While gsr-1a or trxr-2 single mutants are phenotypically normal, double gsr-1a trxr-2 mutants displayed small body size, gonadal migration defects, reduced brood size, and prolonged egg-laying period, without developmental delay or lethality. Transcriptomic analysis revealed strong induction of ATFS-1-dependent stress and detoxification genes. Consistent with this, gsr-1a trxr-2 worms exhibited constitutive ATFS-1 nuclear localization and robust Phsp-6::gfp expression. Triple gsr-1a trxr-2; atfs-1 mutants were nonviable, demonstrating that unfolded protein response (UPRmt) activation is essential under mitochondrial redox stress. Despite the induction of a stress response at the transcriptional level, gsr-1a trxr-2 double mutants were not more resistant to oxidative or pathogen stressors. Moreover, these mutants maintained normal respiration, ATP and ROS production while displaying altered mitochondrial morphology in a tissue-specific manner, independent of mitophagy genes but dependent on mitochondrial fission or fusion machinery. Functionally, gsr-1a trxr-2 mutants showed impaired motility, reduced calcium uptake upon carbachol stimulation, enhanced hypodermal wound repair, and decreased fertilization efficiency associated with lower muscle exopher production. Overall, our data show that simultaneous loss of mitochondrial GSR-1a and TRXR-2 compromises growth, fertility and muscle performance and triggers a constitutive ATFS-1-dependent UPRmt that sustains viability revealing mitochondrial redox control as a core determinant of organismal proteostasis.

Glycolysis inhibition-based breakdown of ferroptosis defenses to achieve ferroptosis and immune cascades for antitumor therapy.

The FOXM1-SESN2 axis maintains redox homeostasis and protects esophageal squamous carcinoma cells from oxidative stress.

ROS-driven rewiring of Hippo-inflammation-polycomb axis by PFOA in 2D and 3D lung epithelial models.

Berberine inhibits muramyl dipeptide-induced oxidative stress and pyroptosis in canine corneal epithelial cells via the NOD2 signaling pathway.

A mitochondria-targeted nanoantioxidant restores alveolar bone homeostasis in periodontitis by quenching ROS and suppressing the cGAS-STING pathway.

Glutathione-deficiency promotes basal hyperinsulinemia in the insulin secreting cell line INS-1 (832/13).

Spermidine alleviates sepsis-induced cardiomyopathy by improving mitochondrial quality and quantity via a Metallothionein 1-dependent antioxidant pathway.