Naunyn Schmiedebergs Arch Pharmacol. 2025 Oct 13. doi: 10.1007/s00210-025-04709-4. Online ahead of print.
ABSTRACT
Vitamin D deficiency is soaring among shift workers due to multiple issues, including poor UVB experience. The objective of this study was to identify precise mechanisms by which vitamin D deficiency might aggravate depressive symptoms among shift workers. Shift work is also associated with disrupting circadian rhythm, leading to depressive symptoms. Differential expressed genes (DEGs) in depression patients (GSE80655, GSE169459, GSE217811, GSE190518, GSE98793, GSE23848, GSE76826, GSE101521, and GSE54572) and in shift workers (GSE122541) with controls were examined in the GEO database. Genes associated with vitamin D deficiency were gathered from the GenCard database. Overlapping core targets were collected by uploading genes into the Bioinformatics and Evolutionary Genomics database. STRING database was used to screen the PPI (protein-protein interaction) network of cross-targets. Cytoscape was used to select core targets and to set up the pathway-gene network. GO (Gene Ontology) enrichment and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway investigations were executed by the database ShinyGO. A molecular docking examination was performed to explain the interaction between protein targets and calcitriol (active form of vitamin D), and binding affinity was confirmed by a 100-ns molecular dynamics simulation study. Our finding designated that the deficit of vitamin D might be involved in the pathology of depression among shift workers mainly through activation of the inflammatory response via upregulation of TNF, IL-6, and IL-1β (pro-inflammatory markers).
PMID:41081792 | DOI:10.1007/s00210-025-04709-4
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