biostudies-literatureRamanathan GNIEHS NIH HHS55https://www.ebi.ac.uk/biostudies/studies/S-EPMC11684268biostudies-literatureUnknown21(1)<h4>Background</h4>Exposure to air pollution is associated with worldwide morbidity and mortality. Diesel exhaust (DE) emissions are important contributors which induce vascular inflammation and metabolic disturbances by unknown mechanisms. We aimed to determine molecular pathways activated by DE in the liver that could be responsible for its cardiometabolic toxicity.<h4>Methods</h4>Apolipoprotein E knockout (ApoE KO) mice were exposed to DE or filtered air (FA) for two weeks, or DE for two weeks followed by FA for 1 week. Expression microarrays and global metabolomics assessment were performed in the liver. An integrated transcriptomic and metabolomic analytical strategy was employed to dissect critical pathways and identify candidate genes that could dissect DE-induced pathogenesis. HepGParticle and fibre toxicologyIntegrated hepatic transcriptomics and metabolomics identify Pck1 as a key factor in the broad dysregulation induced by vehicle pollutants.PMC11684268ES016959, ES029395, ES32806, ES033703Gupta RBhetraratana MRosenfeld MERamanathan GLangmo SLouie AZhao YKaufman JRicks JYang XYin FStewart JAGould TRLarson TVDriscoll WAraujo JAfalseIntegrated hepatic transcriptomics and metabolomics identify Pck1 as a key factor in the broad dysregulation induced by vehicle pollutants.<h4>Background</h4>Exposure to air pollution is associated with worldwide morbidity and mortality. Diesel exhaust (DE) emissions are important contributors which induce vascular inflammation and metabolic disturbances by unknown mechanisms. We aimed to determine molecular pathways activated by DE in the liver that could be responsible for its cardiometabolic toxicity.<h4>Methods</h4>Apolipoprotein E knockout (ApoE KO) mice were exposed to DE or filtered air (FA) for two weeks, or DE for two weeks followed by FA for 1 week. Expression microarrays and global metabolomics assessment were performed in the liver. An integrated transcriptomic and metabolomic analytical strategy was employed to dissect critical pathways and identify candidate genes that could dissect DE-induced pathogenesis. HepG2024-01-01T00:00:00Z2024 Dec2025-04-04T02:26:06.215Z2025-04-04T02:26:06.215ZS-EPMC116842683973420710.1186/s12989-024-00605-6