Search Results (1,002)

The tripeptide glutathione (GSH) is the most abundant cellular non-enzymatic antioxidant. The GSH system plays a crucial role in antioxidant defense against oxidative stress and in supporting cellular redox homeostasis, regulating the reduction of lipid peroxides, and protecting cells from ferroptosis depending on the GSH level, which is maintained in a state of dynamic equilibrium not only by the activities of GSH synthesis enzymes, transporters of GSH precursor amino acids, and GSH transporters, but also by the actions of GSH-related enzymes. Some GSH-related enzymes are key enzymes with antioxidant functions such as glutathione peroxidases (GPxs), especially GPx4, and glutathione S-transferases (GSTs), which use GSH as a co-substrate for the reduction of hydroperoxides to alcohols, whereas glutathione-specific gamma-glutamyl cyclotransferase 1 (ChaC1) degrades intracellular GSH, so they can correspondingly lead to suppression or induction of ferroptosis. Ferroptosis is characterized by a buildup of lipid peroxides due to excessive lipid peroxidation and iron accumulation, which results from redox imbalance between ferroptosis’s drivers and defense systems, including impaired cellular antioxidant systems, particularly disruptions of GSH metabolism. It appears pertinent to assess the influence on ferroptosis regulation by GSH-dependent enzymes that utilize the GSH pool in diverse ways. This review offers an updated exploration of the roles of GPx4, ChaC1, and GSTs in redox regulation of ferroptosis in cancer cells, with a focus on both the regulation of each enzyme’s activity and their possible interactions, considering the impact on the risk of ferroptosis induction. Full article

Vitamin C (L-ascorbic acid) is an essential micronutrient involved in collagen biosynthesis, redox regulation, immune function, endothelial biology, carnitine synthesis, neurotransmitter metabolism, and non-heme iron absorption. Dietary reference values are designed primarily to prevent deficiency in general populations, but vulnerability to low-vitamin C status may increase during trauma, surgery, chronic inflammation, malignancy, metabolic disease, smoking, poor intake, environmental exposure, and tissue repair. This narrative review synthesizes mechanistic, pharmacokinetic, clinical, and safety evidence on vitamin C as a stress-responsive micronutrient. Evidence is reviewed across tissue repair and wound healing, orthopedic recovery and selected complex regional pain syndrome risk contexts, fatigue, neuropsychiatric vulnerability, cancer-supportive care, vascular homeostasis, dermatologic biology, and preliminary microbiota–gut–brain axis hypotheses. The strength of evidence differs substantially across domains: biochemical functions and deficiency correction are well established, whereas benefits of supraphysiologic oral supplementation in vitamin C-replete patients remain uncertain. Oral nutritional supplementation is distinguished from intravenous pharmacologic ascorbate, with attention to route, formulation, dose division, gastrointestinal tolerance-limited adjustment, and safety monitoring. Because evidence for high-dose oral supplementation remains limited and condition-specific, such use should be individualized, time-limited, and clinician-monitored rather than presented as a population-level recommendation or evidence-defined therapeutic target. Taken together, the clinical value of vitamin C depends on baseline status, patient vulnerability, route, formulation, dosing interval, clinical endpoint, and safety review. Full article

The purpose of this study was to offer a theoretical foundation for the use of curcumin in poultry systems for anti-stress responses. Fourteen-day-old SPF Leghorn embryonic eggs were isolated and digested to produce primary cultured cardiomyocytes for this investigation. The primary cultured cardiomyocytes were divided into three groups: the CK group, serving as the control check; the HS group, which underwent a heat stress challenge; and the HS_Cur group, which was pre-treated with curcumin prior to experiencing heat stress. Twenty hours prior to the heat stress phase, the HS_Cur group received 15 μmol/L of curcumin. The culture medium’s cells and supernatant were extracted. Curcumin has been shown to protect cells against heat stress by drastically inhibiting the release of CK-MB and LDH, reducing the generation of MDA, and improving the potential of the mitochondrial membrane. Heat stress may alter cell proliferation, the base repair process, and cause proteotoxic stress, according to pathway enrichment analysis. Several iron metabolism-related pathways were both shown in CK vs. HS and HS vs. HS_Cur comparisons. Curcumin can promote heme synthesis and improve iron storage and antioxidant capacity by suppressing the expression of FTL, MAP1LC3C, and FXN and increasing the expression of SLC7A11, FTH1, FECH, SQSTM1, and NQO1, according to our subsequent analysis of iron metabolism-related DEGs. Curcumin may protect cells from the toxicity of LIP by inhibiting the expression of ferritinophagy-related genes and increasing the expression of heme production, iron storage, and antioxidant-related genes. Full article

Red blood cells (RBCs) are the most abundant cells in peripheral blood and perform critical functions including oxygen and carbon dioxide transport, acid base buffering, regulation of hemorheology, and modulation of immune signaling. Due to their high content of hemoglobin and labile iron, prolonged exposure to high oxygen tension, membrane enrichment with polyunsaturated fatty acids, and the absence of both nucleus and mitochondria, mature RBCs have limited capacity for damage repair and protein re-synthesis, making them highly susceptible to attack by reactive oxygen species (ROS) and reactive nitrogen species (RNS). Hydrogen peroxide (H₂O₂) and 2,2′-azobis(2-methylpropionamidine) dihydrochloride (AAPH) are the two most commonly used inducers in the in vitro models of RBC oxidative injury: H₂O₂ primarily generates hydroxyl radicals via hemoglobin/ferrous ion-dependent Fenton reactions, simulating acute oxidative stress. AAPH releases peroxyl radicals upon thermal decomposition, mimicking persistent lipid peroxidation in cell membranes. Curcumin, a representative polyphenolic compound derived from turmeric, exerts multiple effects including free radical scavenging, metal ion chelation, membrane stabilization, anti-inflammatory activity, and regulation of redox homeostasis. This review systematically summarizes the pathological basis of RBC oxidative damage and the protective effects of curcumin on membrane systems, antioxidant defenses, morphology, and function, based on the core evidence chain “H₂O₂/AAPH—RBCs—curcumin”, integrating recent experimental findings on H₂O₂, AAPH, blood storage-induced injury, and curcumin formulations. It emphasizes that mature RBCs lack nuclei and mitochondria, and therefore mechanisms such as Nrf2/ARE signaling, HO-1 induction, mitochondrial apoptosis, caspase cascades, and inflammasome activation should not be directly equated with transcriptional regulatory pathways within mature RBCs, but rather interpreted as indirect evidence originating from nucleated cells, erythroid progenitors, or the blood microenvironment. The article further proposes that future research should focus on standardized RBC models, physiologically relevant dosages, nanodelivery systems, and translational applications in blood storage, to facilitate the transition of curcumin’s in vitro antioxidant evidence into clinical transfusion medicine and precision nutritional interventions. Full article

Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a promising therapeutic strategy for cervical cancer. However, the mitochondrial factors governing ferroptosis sensitivity in this malignancy remain incompletely understood. PET117, a conserved mitochondrial protein, has been implicated in mitochondrial homeostasis, yet its role in ferroptosis regulation and cervical cancer pathophysiology is unknown. Here, we report a novel role of PET117 in regulating ferroptosis. PET117 expression was significantly elevated in cervical cancer tissues and loss of PET117 in HeLa cells markedly suppressed erastin- and RSL3-induced ferroptosis. Mechanistically, PET117 deficiency attenuated intracellular reactive oxygen species (ROS) accumulation, lipid peroxidation, and iron overload. Mitochondrial proteomics and RNA-seq revealed extensive remodeling of the mitochondrial proteome and ferroptosis-related transcriptional networks upon PET117 depletion. Notably, integrative analysis of mitochondrial and nascent proteomes identified acyl-CoA synthetase family member 2 (ACSF2) as a downstream target of PET117. These findings establish PET117 as a novel regulator of ferroptosis in cervical cancer, thereby linking mitochondrial function to ferroptosis regulation. Full article

Nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H₂S) were once regarded solely as toxic environmental gases. However, accumulating evidence over the past several decades has established them as the three principal endogenous gasotransmitters that regulate a wide spectrum of physiological and pathological processes. Unlike conventional signaling molecules, gasotransmitters diffuse freely across biological membranes and exert potent biological effects through receptor-independent mechanisms, including redox-sensitive post-translational modifications and modulation of heme-containing proteins. Although the individual functions of NO, CO, and H₂S have been extensively reviewed, emerging studies indicate that these gaseous mediators rarely operate in isolation. Instead, they form a highly integrated signaling network characterized by direct chemical interactions, reciprocal enzymatic regulation, and convergence upon common downstream pathways. In this mini-review, we propose the concept of a “Gasotransmitter Trio Network,” emphasizing the molecular crosstalk among NO, CO, and H₂S as a fundamental determinant of cellular homeostasis. We first summarize the biosynthetic pathways and major signaling mechanisms of the gasotransmitter trio, including S-nitrosylation, persulfidation, and heme-dependent regulation. We then discuss recent advances revealing how interactions among these gases generate novel bioactive intermediates and coordinate redox signaling. Particular attention is given to the emerging roles of gasotransmitters in regulating ferroptosis, autophagy, and mitophagy by modulating iron metabolism, lipid peroxidation, mitochondrial quality control, and antioxidant defense systems. These findings support a unified framework in which gasotransmitters function as master regulators of cellular fate under conditions of physiological and pathological stress. Finally, we highlight recent progress in stimuli-responsive donors, CO-releasing molecules (CORMs), NO-releasing materials (NORMs), H₂S donors, and advanced nanoplatforms that enable spatiotemporally controlled gas delivery. We propose that future therapeutic strategies will increasingly rely on programmable multi-gas systems that recapitulate endogenous gasotransmitter networks. Collectively, this review provides a systems-level perspective on gasotransmitter biology and outlines emerging opportunities for the development of precision gas medicine in cardiovascular, neurodegenerative, inflammatory, metabolic, and malignant diseases. Full article

Zinc/iron-regulated transporter proteins (ZIPs) are involved in the transport of zinc and iron, maintenance of ion homeostasis, and regulation of plant responses to abiotic stresses. Although previous studies have identified members of the ZIP gene family and screened for alkaline-responsive ZIP genes in wild soybean (Glycine soja), the functional implications of these genes under alkaline stress conditions remain to be fully elucidated. The present study aimed to identify the GsZIP7 gene and investigate its regulatory role in Arabidopsis and wild soybean under alkaline stress. The results showed that GsZIP7 was highly expressed in roots and young stems. GsZIP7 exhibited differential expression in response to alkaline stress, zinc deficiency, or iron deficiency in wild soybean. In addition, heterologous expression of GsZIP7 in yeast mutants increased tolerance to iron- and zinc-deficient conditions. Overexpression of GsZIP7 in Arabidopsis resulted in reduced root growth, decreased fresh weight, and a weakened antioxidant defense system. Furthermore, GsZIP7-overexpressing soybean hairy roots showed increased sensitivity to alkaline stress, whereas GsZIP7-RNAi lines exhibited enhanced tolerance. Together, these findings indicate that GsZIP7 negatively regulates alkaline tolerance in plants. Full article

Ferroptosis is an iron-dependent regulated form of cell death characterized by lethal lipid peroxidation and is increasingly implicated in cancer, neurodegenerative diseases, cardiovascular injury, and metabolic disorders. Metformin, a widely prescribed antidiabetic biguanide, exerts pleiotropic effects beyond glucose lowering and has emerged as a context-dependent regulator of ferroptosis. In malignant cells, metformin may enhance ferroptotic susceptibility through activation of AMP-activated protein kinase (AMPK), suppression of mechanistic target of rapamycin (mTOR) signaling and SLC7A11, induction of ferritinophagy, mitochondrial complex I stress, and promotion of lipid peroxidation. Conversely, in normal or stressed non-malignant tissues, metformin may limit ferroptotic injury by activating nuclear factor erythroid 2-related factor 2 (NRF2), supporting glutathione peroxidase 4 (GPX4) and SLC7A11-dependent antioxidant defenses, improving mitochondrial quality control, and stabilizing iron homeostasis. This review synthesizes the molecular basis of this duality, evaluates therapeutic opportunities in oncology and cytoprotection, and outlines biomarker-driven and clinical trial strategies required for translation. Overall, metformin should not be regarded as a universal ferroptosis inducer or inhibitor, but rather as a context-dependent metabolic regulator whose effects are shaped by cell type, dose, exposure duration, transporter expression, iron status, and antioxidant capacity. Full article

Gadolinium [Gd (III)] released from gadolinium-based contrast agents, commonly used in magnetic resonance imaging, may accumulate in organs, altering metal homeostasis. We aimed to clarify Gd (III), iron and other metal accumulation in the kidney and brain, in the short (2 days) and long term (20 weeks), following exposure to gadoteric acid (Gd-DOTA) or free Gd (III). Wistar rats received one dose of Gd (III), Gd-DOTA, or saline. Gd (III) and metal levels in the blood (whole blood, and serum in the case of iron), kidney, and brain, and iron metabolism biomarkers, were assessed. Gd (III) was detectable in the blood, kidney, and brain, at both time points, for both Gd (III) and Gd-DOTA-treated groups. Exposure to free Gd (III) showed a significant Gd (III) accumulation in the kidney, brain and blood in the short term and long term; Gd-DOTA presented significant accumulation only in the short term. Gd-DOTA appears to have faster elimination and minimal brain deposition. Exposure to free Gd (III), but not to Gd-DOTA, led to disturbances in metal homeostasis and in iron metabolism markers (serum ferritin and transferrin saturation), but did not alter tissue iron levels. In summary, the kidney appears as the primary site of accumulation and retention. Despite the safer profile shown by Gd-DOTA in the long term, our data highlight the importance of clarifying the pathophysiological implications of Gd (III) retention and/or accumulation, particularly in vulnerable conditions and repeated exposures. Full article

The increasing threat posed by wheat rust diseases caused by Puccinia spp. necessitates the development of resistance strategies that extend beyond conventional race-specific mechanisms. Although recent reviews (2023–2025) have emphasized gene discovery and genomic approaches, comparatively less attention has been given to the potential roles of metabolic regulation and micronutrient homeostasis in host–pathogen interactions. Here, we present a narrative synthesis of current evidence and propose a conceptual framework in which induced mutagenesis (ethyl methanesulfonate, EMS, and γ-irradiation) serves as a tool for investigating interactions among redox regulation, iron (Fe) homeostasis, and disease resistance. A key component of this framework is the proposed interplay between reactive oxygen species (ROS) signaling and Fe partitioning. Vacuolar iron transporters (VITs), ferritins, and associated transport networks regulate intracellular Fe distribution and may influence Fe availability at the host–pathogen interface, potentially affecting fungal development and host defense responses. This concept of “iron-withholding immunity” may operate alongside ROS-mediated defense processes, linking metabolism with immune function. Observations from mutant wheat populations are broadly consistent with the hypothesis that these processes may contribute to durable adult-plant resistance (APR), which is characterized by reduced disease development, coordinated defense responses, and relative stability across environments. In some studies, Fe-enriched mutant lines have been associated with enhanced expression of pathogenesis-related genes and the occurrence of combined APR and seedling-resistance phenotypes, suggesting possible links between micronutrient homeostasis and immunity. Integration of high-throughput phenotyping with genotype × environment × time (G × E × T) frameworks may further improve our understanding of quantitative resistance and disease-associated traits. Overall, this review highlights the potential importance of nutrient homeostasis, redox regulation, and susceptibility modulation as components of future research aimed at developing climate-resilient and nutritionally improved wheat cultivars. Full article

Cardiac disease represents a major cause of morbidity and mortality in dogs. In human cardiology, iron deficiency is a highly prevalent and clinically relevant comorbidity, contributing to exercise intolerance, symptom burden, and impaired quality of life independently of anemia, while correction with intravenous iron improves function and reduces hospitalization. Iron metabolism in dogs remains poorly characterized and typically considered only in the context of anemia. This study investigated iron metabolism and its regulatory pathways in dogs with cardiac disease, assessing whether alterations in iron handling and availability consistent with an iron-restricted phenotype are present. Hematologic indices, serum iron, total and unsaturated iron-binding capacity (TIBC, UIBC), ferritin, hepcidin, ceruloplasmin, C-reactive protein, and albumin were evaluated in 61 dogs comprising healthy controls, and dogs either with compensated cardiac disease (CCD group) or presenting acute decompensated congestive heart failure (ADCHF group). Dogs with cardiac disease exhibited evidence of systemic inflammation, reduced hematocrit, increased red blood cell distribution width, and decreased circulating iron. Both cardiac groups showed reduced TIBC and UIBC, suggesting decreased transferrin availability and reduced iron transport capacity, whereas ferritin concentrations did not differ between groups. Hepcidin concentrations were lower in CCD and not increased in ADCHF patients, suggesting complex and non-uniform regulation of iron homeostasis rather than a classic hepcidin-driven inflammatory pattern. In dogs with ADCHF, iron-binding capacity was independently associated with indices of cardiac remodeling, and additional correlation between inflammatory markers and iron-related parameters supported an interaction between inflammation, iron handling, and disease severity. Full article

Ferroptosis is a regulated form of cell death characterized by iron-dependent lipid peroxidation and membrane damage, with broad relevance to human disease. Accumulating evidence suggests that ferroptosis is governed by coordinated organelle-level regulation, among which lysosomes have emerged as central hubs. By controlling endolysosomal iron processing, transport, and degradation pathways, lysosomes shape the intracellular distribution and reactivity of iron, thereby modulating iron-driven lipid peroxidation. The acidic, iron-rich microenvironment and limited local antioxidant capacity render lysosomal membranes highly susceptible to oxidative injury, positioning lysosomes as initiation and amplification sites of lipid peroxidation. Meanwhile, lysosome-dependent selective autophagy pathways actively remodel iron homeostasis, lipid metabolism, and cellular antioxidant defenses, thereby dynamically modulating ferroptotic sensitivity. Mitochondria–lysosome crosstalk further redistributes iron, reactive oxygen species, and lipid substrates, linking lysosomal activity to interorganelle control of ferroptosis. Lysosomal stress-responsive signaling also coordinates metabolic adaptation and redox control. This review summarizes and integrates current evidence on lysosome-centered mechanisms that organize iron metabolism, lipid peroxidation, selective autophagy, organelle crosstalk, and stress-responsive signaling during ferroptosis, and further discusses their disease-specific roles, therapeutic potential, and translational challenges. Full article

Background/Objectives: Celiac disease (CD) is a complex multifactorial disorder driven by genetic susceptibility and environmental triggers, with ultra-processed foods (UPFs) acting as potential disruptors of immune homeostasis. This study aimed to characterize the patterns and temporality of UPF consumption in a pediatric population with CD to provide evidence-based insights that can optimize the nutritional quality of a gluten-free diet (GFD) beyond mere gluten avoidance. Methods: A total of 128 children aged 5–14 years were enrolled, comprising a baseline cohort of 48 children newly diagnosed with CD (pre-GFD), 88 patients who had followed a GFD for at least 6 months (post-GFD), including 44 participants from the pre-GFD cohort prospectively re-evaluated after 12 months and 44 additional patients with established GFD adherence and a control group of 36 healthy children (CTRL). Dietary intake was assessed using three-day 24 h recalls. Food processing levels were determined using the NOVA classification system, and adherence to the Mediterranean Diet was evaluated via the KIDMED index. Results: At baseline, UPFs (NOVA 4) were the primary daily energy source for both celiac patients and controls, accounting for over 57% of total caloric intake, peaking during breakfast (~74%) and afternoon snacks (~81%). Longitudinal analysis showed that the nutritional profile and global UPF consumption remained remarkably stable after 12 months on a GFD, though a significant increase in vitamin B6 intake was observed (0.9 ± 0.4 vs. 1.1 ± 0.5 mg; p = 0.034). However, meal-pattern shifts occurred over the 12 months: celiac children significantly reduced their daily intake of culinary ingredients (NOVA 2; p = 0.029) and processed foods (NOVA 3; p = 0.025). Compared to healthy controls, post-GFD patients exhibited significantly lower Vitamin D intakes (4.6 ± 9.4 vs. 6.2 ± 12.3 µg/day; p = 0.008), meeting only 30.8% of the reference intake. Both groups presented inadequate intakes of iron, calcium, folate, magnesium, and zinc. Conclusions: Pediatric celiac patients exhibit a high, deeply ingrained consumption of UPFs that mirrors healthy controls and persists 12 months after starting a GFD. While the GFD alters meal processing dynamics, it fails to resolve baseline micronutrient insufficiencies and is associated with lower dietary vitamin D intake, highlighting the urgent need for targeted nutritional interventions that focus on whole food quality rather than just gluten elimination. Full article

Hepcidin is a multifunctional peptide involved in innate immunity and iron homeostasis, yet its earliest developmental regulation in sturgeons remains poorly understood. Here, we investigated maternal loading and embryonic expression patterns of hepcidin transcripts (hamp) in Siberian sturgeon (Acipenser baerii). RT-qPCR detected hamp transcripts in all 17 unfertilized egg (UFE) batches examined; however, maternally loaded transcript abundance varied markedly among batches, with up to a 14.8-fold difference, indicating substantial heterogeneity in the molecular starting state of embryos. In contrast, female traits, including age, body weight, and condition factor, as well as fertilization rate and hatching success, were not significantly correlated with UFE hamp transcript abundance (Spearman’s rank correlation with BH-FDR adjustment; q > 0.05). Developmental expression analysis from UFE to first hatch was then performed using five developmental series (DevSeries 1–5) that represented relatively high, intermediate, and low UFE baseline levels within the statistically differentiated UFE dataset (Welch ANOVA/Games–Howell post hoc, p < 0.05). The developmental dataset showed significant DevSeries, stage, and DevSeries × stage effects, indicating that embryonic hamp expression profiles differed among DevSeries (two-way ANOVA, p < 0.05). High-loading DevSeries (DevSeries 2 and 4) showed prolonged early persistence followed by later re-elevation, whereas low-loading DevSeries (DevSeries 3 and 5) maintained lower overall abundance but displayed more evident stage-linked increases during embryogenesis. Collectively, these findings show that maternally loaded hamp transcripts are associated with embryonic expression profiles and support the view that maternal transcript abundance provides an initial baseline that should be considered when interpreting early developmental expression profiles of immune- and iron-regulation-related genes in this chondrostean species. Full article

Background/Objectives: Ferroptosis, an iron-dependent cell death driven by lipid peroxidation, is implicated in the pathogenesis of ulcerative colitis (UC). Tryptophan metabolism and its interaction with the aryl hydrocarbon receptor (AhR) and nuclear factor erythroid 2–related factor 2 (Nrf2) axis represent a crucial regulatory network in intestinal homeostasis. This study aimed to investigate whether the probiotic fermentation product postbiotic Nagqu4580 alleviates UC by modulating this network to inhibit intestinal epithelial ferroptosis. Methods: An acute UC model was induced in mice using 4% dextran sodium sulfate (DSS). The therapeutic effects of postbiotic Nagqu4580 were evaluated through disease activity index (DAI), colon length, histopathology, inflammatory cytokines, and intestinal barrier function. Ferroptosis was assessed by measuring lipid peroxidation (MDA, 4-HNE), antioxidant capacity (GSH/GSSG), and expression levels of GPX4 and ACSL4. Serum tryptophan metabolites were profiled using targeted metabolomics, the activation of the AhR/Nrf2 pathway was examined by Western blot, immunofluorescence, and qPCR, and gut microbiota composition was analyzed by 16S rRNA sequencing. Results: Postbiotic Nagqu4580 dose-dependently ameliorated DSS-induced UC in mice, as evidenced by reduced DAI scores, mitigated colon shortening and histological damage, decreased inflammatory cytokines (TNF-α, IL-1β, IL-6), and restored intestinal barrier function by upregulating tight junction proteins (Claudin-1, ZO-1, Occludin). Mechanistically, postbiotic Nagqu4580 inhibited intestinal epithelial ferroptosis by reducing MDA and 4-HNE levels, restoring the GSH/GSSG balance, downregulating ACSL4, and upregulating GPX4. Serum metabolomics revealed that postbiotic Nagqu4580 reshaped tryptophan metabolism, increasing beneficial metabolites such as 5-hydroxyindoleacetic acid (5-HIAA) and decreasing potentially harmful metabolites such as 3-indoxyl sulfate (3-IS). 16S rRNA sequencing further revealed that the postbiotic Nagqu4580 partially reversed DSS-induced gut microbiota dysbiosis, with a slight increase in the abundance of beneficial genera and a significant reduction in the abundance of pro-inflammatory genera. Furthermore, postbiotic Nagqu4580 significantly activated the AhR/Nrf2 signaling pathway, enhancing the expression of AhR, Nrf2, and their downstream antioxidant genes HO-1 and GPX4. Conclusions: Postbiotic Nagqu4580 alleviates UC by inhibiting intestinal epithelial ferroptosis. Our data suggest that this protective effect is associated with the remodeling of gut microbiota-related tryptophan metabolism and subsequent activation of the AhR/Nrf2 antioxidant axis. Our findings highlight the therapeutic potential of postbiotic Nagqu4580 as a postbiotic agent for UC. Full article