<HashMap><database>iProX</database><scores/><additional><omics_type>Proteomics</omics_type><submitter>Fu Gao</submitter><species>Homo Sapiens</species><full_dataset_link>http://www.iprox.org/page/project.html?id=IPX0012626000</full_dataset_link><submitter_email>gaof@im.ac.cn</submitter_email><submitter_affiliation>Institute of Microbiology, Chinese Academy of Sciences</submitter_affiliation><sample_protocol></sample_protocol><repository>iProX</repository><data_protocol></data_protocol></additional><is_claimable>false</is_claimable><name>Proteomic characteristics of diabetic patients infected with SARS-CoV-2 Omicron variant</name><description>We comprehensively characterized alterations in the serum proteome through proteomic analysis. A total of 2,297 high-confidence proteins were identified. Principal Component Analysis (PCA) based on protein expression levels revealed inter-sample relationships across multiple dimensions. The results demonstrated distinct clustering patterns between mild and severe infection groups in protein expression profiles. Partial overlap was observed between diabetes-associated mild and severe infection groups. Pairwise comparisons revealed distinguishable proteomic signatures among all groups. Differential analysis identified 1,325 statistically significant proteins between severe and mild cases. These comprised approximately 1,000 upregulated and 397 downregulated proteins. Prominent upregulated proteins in severe cases included SH3KBP1, FCER1G, FUBP1, LAMP1, GSDMD, RPL36, RBX1, CAPG, CPPED1, and SAMSN1. Significant downregulation was observed in AEBP1, BCHE, TRPM2, PRSS3, SMU1, SFRP4, SPOCK3, PHF14, UNC13B, and CTSV. These proteomic alterations indicate a hyperactivated stress response in severe patients. Enhanced immune-inflammatory activation co-occurred with suppressed cellular repair and metabolic regulation. Such dysregulation may exacerbate inflammatory tissue damage, cellular apoptosis, and multi-organ dysfunction. This pathophysiological cascade underlies the development of severe clinical complications.</description><dates><publication>Tue Aug 05 00:00:00 BST 2025</publication></dates><accession>PXD066966</accession><cross_references><TAXONOMY>9606</TAXONOMY></cross_references></HashMap>