{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang Z"],"funding":["STI2030-Major Projects","Shanghai Municipal Commission of Science and Technology Program","Shanghai Education Commission Research and Innovation Program"],"pagination":["2183"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12467129"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(9)"],"pubmed_abstract":["<b>Background:</b> Major depressive disorder (MDD) is a prevalent and disabling psychiatric illness with complex etiologies involving both genetic and environmental factors. While environmental stress is a known risk factor of MDD, the molecular mechanisms linking stress exposure to persistent depressive phenotypes remain incompletely understood. <b>Methods</b>: We established a 24-hour restraint stress-induced depression model in mice and performed integrated transcriptomic and proteomic analyses of the medial prefrontal cortex (mPFC) to investigate stress-related molecular alterations. <b>Results</b>: Behavioral assessments confirmed persistent depression-like phenotypes, including anhedonia and behavioral despair, lasting up to 35 days post-stress. RNA sequencing identified differentially expressed genes related to dopaminergic signaling and oxidative stress. Proteomic analysis identified 105 differentially expressed proteins involved in immune response and energy metabolism. Integrated multi-omics analysis highlighted convergent disruptions in immune regulation, metabolism, and epigenetic processes. Notably, clemastine exerts its antidepressant-like effects in part by mitigating neuroinflammation and preserving mitochondrial function. <b>Conclusions</b>: These findings provide novel insights into the molecular basis of stress-induced depression and suggest that clemastine is a potential therapeutic candidate."],"journal":["Biomedicines"],"pubmed_title":["Integrated Multi-Omics Analysis Reveals Immune and Metabolic Dysregulation in a Restraint Stress-Induced Depression Model."],"pmcid":["PMC12467129"],"funding_grant_id":["2022ZD0204900","2019-01-07-00-02-E00037","23490712600"],"pubmed_authors":["Li W","Li Y","Zhao Q","Wang X","Wang Z","Lan Z"],"additional_accession":[]},"is_claimable":false,"name":"Integrated Multi-Omics Analysis Reveals Immune and Metabolic Dysregulation in a Restraint Stress-Induced Depression Model.","description":"<b>Background:</b> Major depressive disorder (MDD) is a prevalent and disabling psychiatric illness with complex etiologies involving both genetic and environmental factors. While environmental stress is a known risk factor of MDD, the molecular mechanisms linking stress exposure to persistent depressive phenotypes remain incompletely understood. <b>Methods</b>: We established a 24-hour restraint stress-induced depression model in mice and performed integrated transcriptomic and proteomic analyses of the medial prefrontal cortex (mPFC) to investigate stress-related molecular alterations. <b>Results</b>: Behavioral assessments confirmed persistent depression-like phenotypes, including anhedonia and behavioral despair, lasting up to 35 days post-stress. RNA sequencing identified differentially expressed genes related to dopaminergic signaling and oxidative stress. Proteomic analysis identified 105 differentially expressed proteins involved in immune response and energy metabolism. Integrated multi-omics analysis highlighted convergent disruptions in immune regulation, metabolism, and epigenetic processes. Notably, clemastine exerts its antidepressant-like effects in part by mitigating neuroinflammation and preserving mitochondrial function. <b>Conclusions</b>: These findings provide novel insights into the molecular basis of stress-induced depression and suggest that clemastine is a potential therapeutic candidate.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-05-02T03:10:57.68Z","creation":"2026-05-02T03:07:50.669Z"},"accession":"S-EPMC12467129","cross_references":{"pubmed":["41007746"],"doi":["10.3390/biomedicines13092183"]}}