GEOTranscriptomicsRattus norvegicusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE298727GEOGSEfalseNADPH Oxidase 4 and Metabolic Stress in Dahl Salt-Sensitive Rat KidneysThis study investigated how redox regulation influences renal metabolic reprogramming induced by high salt (HS) intake, by comparing Dahl salt-sensitive (SS) rats and SS rats deficient in NADPH oxidase 4 (SSNOX4⁻/⁻). In SS rats, HS intake upregulated glutaminase and increased glutamate consumption, reflecting a shift toward glutamine-driven metabolism, inefficient oxygen utilization, and elevated ROS. In contrast, SSNOX4⁻/⁻ rats exhibited intrinsically higher NO production and favored fatty acid oxidation (FAO), promoting more efficient oxygen. Notably, renal lactate release was observed exclusively in SSNOX4⁻/⁻ rats following HS intake, despite no glycolytic gene upregulation, suggesting increased lactate production due to a substrate shift, possibly toward enhanced FAO. Furthermore, SSNOX4⁻/⁻ rats did not exhibit the salt-induced augmentation of amino acid metabolism seen in SS rats, indicating a protein-sparing metabolic adaptation. Together, these findings reveal a distinct metabolic reprogramming in SSNOX4⁻/⁻ rats that enhances energy efficiency and contributes to renal protection under HS conditions.2026/05/07GSE298727GSM9021638GSM9021639GSM9021678GSM9021634GSM9021635GSM9021679GSM9021636GSM9021637GSM9021641GSM9021685GSM9021642GSM9021686GSM9021687GSM9021643GSM9021644GSM9021688GSM9021681GSM9021682GSM9021683GSM9021684GSM9021640GSM9021680GSM9021649GSM9021645GSM9021689GSM9021646GSM9021647GSM9021648GSM9021652GSM9021653GSM9021654GSM9021655GSM9021650GSM9021651GSM9021690GSM9021691GSM9021656GSM9021657GSM9021658GSM9021659GSM9021663GSM9021664GSM9021665GSM9021666GSM9021660GSM9021661GSM9021662GSM9021667GSM9021668GSM9021669GSM9021674GSM9021675GSM9021632GSM9021676GSM9021633GSM9021677GSM9021670GSM9021671GSM9021672GSM902167325947298727Rattus norvegicus[41368709]