Search Results (1,050)

Glucose-6-phosphate dehydrogenase (G6PD) deficiency impairs NADPH generation through the pentose phosphate pathway, resulting in reduced glutathione regeneration and increased vulnerability to oxidative stress. While its clinical significance is well described in hemolytic disorders, its impact on tumor biology and chemosensitivity remains poorly characterized. Cisplatin, a backbone agent in the management of nasopharyngeal carcinoma (NPC), exerts its cytotoxicity through the formation of DNA adducts and the robust induction of reactive oxygen species (ROS) activity. We report a patient with non-keratinizing NPC and a G6PD variant, a (class III) deficiency, who demonstrated a rapid and pronounced objective response to cisplatin-based induction and concurrent chemoradiotherapy. Unfortunately, the patient also exhibited signs of rapid and persistent hematologic (platelets and white cells) toxicity. Notably, no hemolytic events occurred. A narrative review of the available literature indicates that G6PD-deficient cells exhibit a reduced antioxidant reserve, increased cisplatin-induced DNA damage, and impaired activation of ROS-detoxifying pathways. A few clinical observations similarly report enhanced tumor responsiveness in G6PD-deficient individuals, although the evidence is sparse and heterogeneous. Preclinical data support the notion that diminished NADPH availability amplifies cisplatin-triggered oxidative injury, thereby increasing tumor susceptibility. This case adds to emerging evidence that G6PD deficiency may potentiate cisplatin efficacy in NPC by exploiting intrinsic redox vulnerabilities. While preliminary, these findings suggest the potential utility of metabolic phenotyping in treatment stratification. Prospective studies are needed to define the predictive value, safety, and therapeutic implications of G6PD status in cisplatin-based regimens. Full article

Peritoneal dialysis (PD) is limited by insufficient phosphate removal, leading to adverse cardiovascular outcomes in patients with chronic kidney disease. To advance the understanding of the molecular mechanisms of peritoneal phosphate transport, RNAseq data of phosphate transporters in four PD-relevant cell lines were analyzed. The expression and localization of the respective proteins were validated by immunostaining in these cells. The transcriptomics of omental arterioles from children on PD were analyzed. In vitro Transwell models of an immortalized mesothelial cell line (MeT-5A) and human umbilical vein endothelial cells (HUVECs) and respective co-cultures were established, enabling quantification of phosphate transport across mesothelial and endothelial monolayers. Sodium phosphonoformate tribasic hexahydrate (PFA) and Tenapanor were used to inhibit transcellular and paracellular transport pathways. Cell viability and integrity markers were measured over the experimental periods. SLC20A1 and SLC20A2 were expressed across all studied cell types, while SLC34A2 and SLC34A3 were mesothelial cell-specific. Omental arterioles of children on low-glucose-degradation-product (GDP) PD showed higher SLC20A1 expression vs. stage 5 chronic kidney disease (CKD5) and healthy controls. Permeability for phosphate was lower across MeT-5A compared with HUVEC monolayers and was not further reduced in co-culture. Inhibitors reduced both transcellular and paracellular transport to 75% in MeT-5A and 65% in co-cultures, while no effects were observed in HUVEC alone, suggesting the mesothelial cell layer as a significant barrier for phosphate transport. Our studies provide first analyses combining findings on molecular phosphate transporters in peritoneal cells and arterioles and introducing a Transwell model for quantitative studies of phosphate kinetics. Full article

Sea urchins are invertebrates that play a crucial role in marine ecosystems by controlling benthic algal communities and whose natural populations are being affected by different biotic and abiotic factors. Triggering physiological processes promotes the activation of certain metabolic pathways, so oxidative status markers could be a suitable tool to asses maturation stage in which natural populations are. Antioxidant status of three species of Mediterranean Sea urchins, A. lixula, P. lividus and S. granularis, was evaluated in gonadal and digestive tissue. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione s-transferase (GST), glucose 6-phosphate dehydrogenase (G6PDH), NAD(P)H: quinone oxidoreductase (NQO1) and lipid peroxidation were assayed. Significant differences were found among species, displaying in general higher antioxidant activity in A. lixula and S. granularis compared to P. lividus. A significant effect of sex was observed with females exhibiting a higher gonadosomatic index and higher levels of lipid peroxidation mainly in A. lixula. These results seem to be related to metabolic fluctuations associated with the gonadal maturation stage. Changes in digestive tissue were less evident, but some differences among species could be related to triggered digestive processes for replenishment of energy reserves in gonads. Oxidative status can be a useful complementary tool to evaluate gonadal condition in species of sea urchin from the same habitat. Integrative physiological and biochemical studies will contribute to the knowledge of invertebrate physiology. Full article

A nanostructured sensing platform based on electrospun functionalized multi-walled carbon nanotubes/poly(3-aminobenzylamine) (FMWCNTs/P3ABA) was developed for the electrochemical detection of dopamine (DA) on fluorine-doped tin oxide (FTO) glass substrate. The electrochemical characteristics of the electrodes were investigated by chronocoulometry (CC) and cyclic voltammetry (CV) in phosphate-buffered saline solution containing K₃[Fe(CN)₆] as a redox mediator. The zeta potential analysis confirmed the presence of a stable surface charge that favors electrostatic interaction with DA molecules. The DA detection was performed in human urine by differential pulse voltammetry (DPV) over a potential of −0.2 to 0.8 V and at scan rate of 5 mV s⁻¹, where the FMWCNTs/P3ABA nanofiber electrode exhibited a high sensitivity of 1.502 µA cm⁻² nM⁻¹, a linear detection range of 10–500 nM (R² = 0.992), and a limit of detection of 1.753 nM. The sensor exhibited stable and reproducible responses, and the fibrous composite effectively discriminated DA from common electroactive interferents, including ascorbic acid, uric acid, creatinine, and glucose. Furthermore, reliable dopamine quantification in human urine samples demonstrates the strong potential of the electrospun FMWCNTs/P3ABA composite nanofiber platform for practical bioanalytical and non-invasive sensing applications in the future. Full article

Background: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is among the most common inherited enzymatic disorders worldwide and is an important risk factor for neonatal hyperbilirubinemia. Regional data from Western Saudi Arabia based on universal newborn screening remain limited. Objectives: To determine the prevalence of G6PD deficiency among newborns delivered at a tertiary center in Jeddah, Saudi Arabia, and to evaluate its association with clinically relevant outcomes, including early-onset jaundice (<24 h), need for phototherapy, admission for hyperbilirubinemia management, and readmission after discharge. Methods: We conducted a retrospective cohort study at King Abdulaziz Medical City, Western Region, Jeddah, Saudi Arabia, between January 2020 and May 2025. Cord blood samples from live-born infants were screened using a qualitative fluorescent spot test. Demographic variables (sex, gestational age, birth weight) and jaundice-related outcomes were extracted from the electronic medical record. Categorical variables were compared using chi-square testing, with p < 0.05 considered statistically significant. Results: Among 14,964 screened newborns, 489 were identified as G6PD deficient, yielding a prevalence of 3.3%. Prevalence was higher in males than in females (5.6% vs. 0.9%). Among the G6PD-deficient infants, early-onset jaundice occurred in 17.2%, phototherapy was required in 36.0%, and 16.5% were admitted for hyperbilirubinemia management. Readmission for worsening jaundice requiring phototherapy occurred in 11.0%, and no exchange transfusions were required. Compared with term infants, late preterm infants had higher rates of early-onset jaundice (11/49, 22.4% vs. 73/440, 16.6%) and phototherapy use (22/49, 45.0% vs. 154/440, 35.0%) (p < 0.01). Conclusions: G6PD deficiency was identified in a substantial proportion of newborns in this large screened cohort and was associated with clinically significant jaundice-related outcomes, particularly among late preterm infants. These findings underscore the importance of universal screening and structured postnatal follow-up to reduce the risk of severe hyperbilirubinemia and its complications. Early identification of G6PD-deficient infants should be accompanied by careful bilirubin monitoring, clear discharge planning, and timely post-discharge follow-up, especially for those born late preterm. Full article

The global rise in the incidence and severity of invasive fungal infections, particularly among immunocompromised and immunodeficient patients, has created an urgent need for rapid and accurate diagnostic techniques. Therefore, fungal-specific positron emission tomography imaging agents are increasingly in demand, as they offer the potential for early-stage detection of fungal infections. Recently, 2-deoxy-2-[¹⁸F]fluorocellobiose ([¹⁸F]FCB), a fluorine-18-labeled analog of cellobiose that is selectively metabolized by fungal pathogens possessing cellulose-degrading mechanisms (cellulolytic), was developed for the targeted imaging of Aspergillus infections. However, the final [¹⁸F]FCB contained less than 2% unreacted 2-deoxy-2-[¹⁸F]fluoroglucose ([¹⁸F]FDG), which can potentially interfere with image interpretation. Accordingly, this study aims to eliminate residual [¹⁸F]FDG from the final product by enzymatically converting it to [¹⁸F]FDG-6-phosphate through hexokinase-mediated phosphorylation. A Trasis AllInOne (Trasis AIO) module was used to automate the radiolabeling procedure. The reagent vials contain [¹⁸F]FDG, glucose-1-phosphate, cellobiose phosphorylase, adenosine triphosphate (ATP), and hexokinase. A Sep-Pak cartridge was used to purify the tracer. The overall radiochemical yield was 45–50% (n = 3, decay-corrected) in a 40 min synthesis time, with a radiochemical purity of >99% (no detectable [¹⁸F]FDG). This is a highly reliable protocol to produce current good manufacturing practice (cGMP)-compliant [¹⁸F]FCB for clinical PET imaging. Full article

Naked oat (Avena nuda L.) is an important dual-purpose crop for grain and forage in cold regions; however, its high fatty acid content renders seeds prone to deterioration during storage. This study aimed to investigate the protective effects of zinc oxide nanoparticles (ZnO NPs) on artificially aged naked oat seeds and elucidate the underlying molecular mechanisms. Non-aged seeds (Naged) were subjected to artificial aging at 45 °C and 100% relative humidity for 24 h (Aged), followed by priming with 30 mg L⁻¹ ZnO NPs for 6 h (Daged). Antioxidant enzyme activities were determined spectrophotometrically, and transcriptome sequencing was performed on an Illumina platform to identify differentially expressed genes (DEGs) and enriched pathways. We found that ZnO NPs increased catalase (CAT), peroxidase (POD) and superoxide dismutase (SOD) activities by 3–4-fold, restored germination rate from 75% to 98%, and enhanced seed vigor index. A total of 21,403 DEGs were detected, with 15,841 stably expressed in response to nano-priming. Reactive oxygen species (ROS) burst rapidly induced up-regulation of AP2/EREBP transcription factor family members, which subsequently activated antioxidant enzyme genes to maintain cellular redox homeostasis. Metabolic pathway analysis demonstrated that the phenylpropanoid pathway was reprogrammed, characterized by down-regulated lignin biosynthesis and up-regulated flavonoid production, thereby enhancing ROS scavenging capacity. Additionally, the pentose phosphate pathway was activated to provide additional NADPH for antioxidant defense, and up-regulated ADP-glucose pyrophosphorylase (AGPase) facilitated starch accumulation. Notably, the 40S ribosomal protein S13 exhibited the highest connectivity in protein–protein interaction networks, was up-regulated 2.1-fold, and was enriched in post-translational modification processes. These findings suggest that nano-priming with ZnO NPs represents a promising biotechnological strategy for enhancing seed vigor and storability in naked oat, with potential applications in sustainable agriculture and the seed industry. Full article

It is widely recognized that microbial inoculants (MI) and bio-organic fertilizers (BOFs) containing beneficial microorganisms can play an important role in improving orchard soil properties and enhancing fruit quality. However, insufficient data regarding the relevant fruit quality effects hindered the supplementary MI and BOFs in kiwifruit cultivation. Using conventional fertilization management as the control, this study investigated the impacts of supplementary applications of MI and BOFs at two gradient dosages on the harvest-time quality and cold storage characteristics of ‘Puyu’ yellow-fleshed kiwifruit. Regarding leaf physiological indices and soil pH, MI-3.0 and BOF-20 treatments significantly elevated total chlorophyll content at 60 days after flowering (DAF) (the fruit expansion stage). Leaf nitrogen (N), phosphorus (P) and potassium (K) contents declined gradually during fruit development, while MI-2.0 and BOF-10 treatments markedly promoted leaf P accumulation at 20–100 DAF. Additionally, the MI-2.0 treatment significantly reduced 20–40 cm subsoil pH, which is favorable for kiwifruit plants that prefer acidic and slightly acidic conditions. On the other hand, appropriate doses of MI and BOF treatments exerted a significant effect on improving the quality of kiwifruit at the ripening stage. These effects were mainly manifested in the increased single fruit weight, firmness, dry matter content and total soluble solids (TSSs) of kiwifruit following MI-3.0 and BOF-20 treatments. Furthermore, MI-3.0 and BOF-10 notably elevated the fructose and glucose contents in both flesh and core, as well as sucrose and ascorbic acid (AsA) contents in the flesh; MI-2.0 and BOF treatments significantly increased citric and malic acids in the core and quinic acid in the flesh. During cold storage, the BOF-20 treatment not only delayed the occurrence of the ethylene peak by 20 d and significantly reduced its peak value, but also alleviated the decline in total acid content at the middle storage stage (20–40 d). Additionally, MI-2.0 and BOF-20 treatments effectively delayed kiwifruit softening at the early storage stage (0–10 d), and MI treatments maintained a high AsA content in the core during 10–20 d of cold storage. MI and BOF fertilization treatments had little effect on the dynamic change trends of sucrose synthase (SuS), sucrose phosphate synthase (SPS) and acid invertase (AI) in kiwifruit during cold storage, only exerting significant effects at specific time points. In conclusion, supplementary applications of MI and BOFs could improve kiwifruit quality at the harvest stage by positively regulating the accumulation of dry matter, soluble sugars and organic acid contents, and also have the potential to enhance the storage performance of kiwifruit. These findings provide a scientific basis for establishing an effective fertilization regime for kiwifruit. Full article

Soil hypoxia caused by waterlogging severely restricts kiwifruit growth, and screening waterlogging-tolerant rootstocks and analyzing their mechanisms are of great significance for industrial development. In this study, waterlogging-tolerant Actinidia valvata ‘Shuixiu’ was used as the test material and Actinidia chinensis ‘Hongyang’ as the control. Waterlogging stress was simulated artificially, and physiological measurements combined with transcriptome sequencing were used to explore its waterlogging tolerance regulatory characteristics based on respiratory metabolism. The results showed that the waterlogging tolerance of ‘Shuixiu’ was significantly better than that of ‘Hongyang’. It upregulated sucrose synthase and α/β-amylase genes and inhibited the continuous up-regulation of trehalose-6-phosphate synthase genes, leading to significant accumulation of glucose-6-phosphate, a key glycolytic substrate. Some members of glycolytic key gene families, such as glucose-6-phosphate isomerase and phosphofructokinase, were upregulated in ‘Shuixiu’, which increased phosphoglycerate kinase activity and accumulated 3-phosphoglyceric acid and pyruvate, ensuring efficient conversion of carbon sources to ATP. Some members of core tricarboxylic acid cycle gene families, such as pyruvate dehydrogenase and citrate synthase, were upregulated in ‘Shuixiu’, with significantly higher pyruvate dehydrogenase activity and acetyl coenzyme A content, maintaining partial aerobic respiration capacity. Some members of the alanine transaminase gene family were upregulated in ‘Shuixiu’ to enhance alanine fermentation, resulting in a significant reduction in root ethanol accumulation. This study clarified the core respiratory metabolic regulatory characteristics of kiwifruit in response to waterlogging and provided key targets and a theoretical basis for molecular breeding of waterlogging-tolerant rootstocks. Full article

Glucosamine (GlcN) is an essential amino monosaccharide widely used in pharmaceuticals, nutraceuticals, and cosmetics. Microbial fermentation presents a sustainable alternative to its traditional chemical production. However, in Saccharomyces cerevisiae, competitive carbon flux towards ethanol significantly limits GlcN yields. In this study, an S. cerevisiae strain for GlcN biosynthesis was engineered by integrating heterologous GlmD (glucosamine-6-phosphate deaminase) and GlmP (glucosamine-6-phosphate phosphatase) genes. To redirect carbon flux, the pyruvate decarboxylase genes pdc1, pdc5, and pdc6 were sequentially knocked out using the Clustered Regularly Interspaced Short Palindromic Repeats Cas9 (CRISPR-Cas9) approach, generating strains S. cerevisiaeGlmDP/pdc1Δ, GlmDP/pdc1Δpdc5Δ, and GlmDP/pdc1Δpdc5Δpdc6Δ. S. cerevisiae GlmDP/pdc1Δpdc5Δpdc6Δ achieved a GlcN titer of 2.20 ± 0.11 g/L, a 1.54-fold increase over the parental S. cerevisia GlmDP strain, while its ethanol yield decreased by 26%. This enhancement was achieved without significantly affecting cell growth or glucose consumption. Comparative transcriptomics between the triple-knockout and parental yeasts revealed 892 differentially expressed genes. Pathways related to glycolysis and ethanol formation were predominantly downregulated, whereas pathways potentially supporting GlcN synthesis were upregulated. The engineered strain demonstrated high genetic stability over 50 generations. Our findings demonstrate that disrupting ethanol formation is an effective strategy to enhance GlcN production in S. cerevisiae, providing valuable insights for carbon flux redistribution. Full article

Erythroid acute myeloid leukemia (AML) cell line OCI-M2 expresses a particular oncogenic network: IRF6, in concert with ETV2 and HEY1, aberrantly activates NKL homeobox gene NKX2-4, which in turn represses megakaryocytic lineage factor FLI1. Interestingly, in keratinocytes, IRF6 is able to bind glucose which promotes IRF6-dimerization and thus alters its binding site selection. Here, we used OCI-M2 as a model to investigate the role of glucose level and IRF6 in leukemogenesis. Treatment of OCI-M2 with high glucose or 2-deoxy-glucose resulted in the downregulation of IRF6 and NKX2-4, and the upregulation of FLI1, indicating that glucose-mediated dimerization of IRF6 altered its reported autoactivation. The screening of this cell line for genes encoding glycolytic enzymes identified aberrant overexpression of glucose-6-phosphate isomerase (GPI) and phosphofructokinase L (PFKL), which were targeted by genomic amplification and chromothripsis-like alterations, respectively. Furthermore, GPI was activated by NKX2-4 and ETV2, and PFKL by ETV2. Finally, siRNA-mediated downregulation of PFKL resulted in elevated glucose levels, suppressed expression of IRF6 and NKX2-4, and activated FLI1. Thus, we connected an oncogenic regulatory network with deregulated glycolytic enzymes and glucose metabolism, thereby establishing a new in vitro model to develop novel therapeutic avenues in AML subsets. Full article

The global prevalence of obesity continues to rise, posing serious risks to human health largely because obesity itself leads to metabolic disorders of carbohydrate and lipids. Currently, effective and healthy interventions for lowering blood glucose, reducing blood lipids, and promoting weight loss remain limited due to the complexity of obesity development. Lactobacillus plantarum (GDMCC 1.140) was shown to promote catabolic processes and reduce hepatic lipid accumulation in largemouth bass fed with high-starch feed (HSF) in our previous study; however, molecular mechanisms underlying the function of this probiotic remain unclear. Here, we evaluated the effects of L-carnosine, one of metabolites produced by Lactobacillus plantarum, on carbohydrate and lipid metabolisms in an obesity model of zebrafish, which was induced by HSF. Histopathological analyses of livers from different groups indicated that a dietary supplement with L-carnosine can alleviate hepatic impairment and reduce lipid accumulation in the hepatocytes of obese zebrafish. Transcriptomic analyses revealed that L-carnosine supplementation can reverse the expression of about 70 HSF-induced genes, mainly gene-specific transcription regulators and metabolite interconversion enzymes. Furthermore, approximately 250 HSF-inhibited genes were found to be up-regulated by L-carnosine, reaching levels comparable to those in normal-starch feed (NSF) zebrafish. These genes, targeted by L-carnosine and inhibited by HSF, are highly enriched in GO terms such as lipid metabolic process, small molecule metabolic process, and cellular response to chemical stimulus, with monocarboxylic acid metabolic process, modified amino acid metabolic process and aldehyde metabolic process following, and in KEGG pathways of carbohydrate, lipid and amino acid metabolisms, such as pentose and glucuronate interconversions, glycolysis/gluconeogenesis, glycerolipid metabolism, pentose phosphate pathways, fatty acid degradation, beta-alanine metabolism and arginine and proline metabolism. These findings provide functional and molecular evidence that L-carnosine can ameliorate HSF-induced disorders of carbohydrate and lipid metabolisms. Full article

Renal cell carcinoma (RCC) is the most common kidney cancer, with increasing global incidence. Despite advances with VEGF-targeted tyrosine kinase inhibitors (TKIs) and immunotherapies, therapeutic resistance remains frequent, limiting long-term benefits. This highlights the need for potential biomarkers of tumor aggressiveness and therapeutic candidates, such as glucose-6-phosphate dehydrogenase (G6PD), whose altered expression has been associated with several cancers. We evaluated G6PD gene and protein expression in 121 RCC samples through immunohistochemistry and assessed functional role in vitro approaches. 786-O and ACHN cells were treated with the inhibitor G6PDi-1 and the anti-VEGF cabozantinib/lenvatinib. G6PD mRNA levels were higher in tumors than in non-neoplastic tissues, indicating shorter overall survival in clear cell (ccRCC) and papillary (pRCC) subtypes. Immunolabeling confirmed a higher expression in pRCC and associations with pathological features. CRISPR and RNAi datasets revealed a stronger G6PD dependency in the ccRCC. A high gene expression was observed in lenvatinib non-responder cell lines, and DepMap dose–response curves indicated modest responses to VEGF inhibitors. In vitro, ACHN was more sensitive to VEGF inhibition, particularly cabozantinib, whereas G6PDi-1 had stronger effects in 786-O, impairing viability, migration, and clonogenic capacity. Our findings support G6PD as a biomarker of tumor aggressiveness and G6PDi-1 as a potential therapeutic in RCC models. Full article

Background/Objectives: Gamma-aminobutyric acid (GABA) is a bioactive, non-proteinaceous amino acid with potential health benefits. Weissella cibaria UF-274 is an important lactic acid bacterium isolated from Balinese fermented sausage (urutan) with GABA-producing abilities. The aim of this study was to enhance GABA synthesis in skim milk as a basal substrate, as well as whole genome sequencing and analysis to evaluate the functionality and safety of the strain. Methods: A Box–Behnken response surface design was used to enhance GABA accumulation in skim milk. Results: The optimum conditions for GABA production were at concentrations of glucose of 23.91 g/L, monosodium glutamate concentrations of 2.32 g/L and pyridoxal-5′-phosphate at 46 μM. The genome assembly produced a high-quality draft with a 2.53 Mb circular chromosome and 2378 coding sequences. A whole genome analysis revealed that the strain possesses a glutamine amidotransferase (puuD-like) as an alternative route linked to the GABA pathway. AntiSMASH prediction results showed that the strain has two biosynthetic gene clusters including terpene and type III polyketide synthases. Several bioinformatic approaches predicted no antibiotic resistance genes, while van genes encoding vancomycin resistance were detected with low pathogen risk with one approach. Conclusions: Weissella cibaria UF-274 is a promising GABA producer with genomic evidence and a good candidate for functional food development. Full article

Vesicular stomatitis virus (VSV) is a promising oncolytic virus whose replication efficiency and tumor selectivity are strongly influenced by host cell metabolism. Cancer cells, including glioblastoma, exhibit profound rewiring of central carbon metabolism to sustain proliferation, redox balance, and biosynthetic demand, yet how these metabolic states regulate VSV replication remains incompletely defined. Here, we investigated the dependency of VSV replication on glycolysis, the pentose phosphate pathway (PPP), and glutamine metabolism in A172 human glioblastoma cells. Pharmacologic inhibition of glycolysis using 2-DG strongly suppressed VSV replication in a dose-dependent manner, highlighting a robust requirement for glycolytic flux and downstream intermediates. While inhibiting the PPP with 6-AN, a nicotinamide adenine dinucleotide (NAD) analog, markedly impaired viral replication, D-ribose was unable to rescue the inhibition, indicating that nucleotide precursor limitation alone was insufficient to explain this effect. Interestingly, depletion of glucose 6-phosphate dehydrogenase (G6PD), a key enzyme in the PPP, resulted in significant enhancement of VSV replication. Restoration of viral replication by NAD⁺ precursors in the presence of 6-AN or suppression of replication by the NAMPT inhibitor FK866 suggested NAD⁺ availability as a critical determinant of VSV replication. Additionally, blockade of glutaminase activity with BPTES reduced viral replication, underscoring the importance of anaplerotic pathways in glioblastoma cells. Collectively, these findings demonstrate that VSV replication is tightly coupled to metabolic programs, particularly those governing energy production and NAD(P)H balance. This work provides a metabolic framework for optimizing oncolytic VSV therapies and suggests that metabolic interventions in cancer treatment may influence oncolytic virus efficacy. Full article