Academic Journal

Integrated Bioinformatics and Experimental Validation to Identify Shared Sialylation-Related Signatures in Emphysematous and Fibrotic Lung Disease.

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: Integrated Bioinformatics and Experimental Validation to Identify Shared Sialylation-Related Signatures in Emphysematous and Fibrotic Lung Disease.
Συγγραφείς: Wang Y; Department of Respiratory and Critical Care Medicine, Beijing Institute of Respiratory Medicine and Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China., Cao K; Department of General Surgery, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China., Zhao W; Department of Occupational Medicine and Toxicology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Πηγή: FASEB journal : official publication of the Federation of American Societies for Experimental Biology [FASEB J] 2026 Sep 30; Vol. 40 (18), pp. e72302.
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Federation of American Societies for Experimental Biology Country of Publication: United States NLM ID: 8804484 Publication Model: Print Cited Medium: Internet ISSN: 1530-6860 (Electronic) Linking ISSN: 08926638 NLM ISO Abbreviation: FASEB J Subsets: MEDLINE
Imprint Name(s): Publication: 2020- : [Bethesda, Md.] : Hoboken, NJ : Federation of American Societies for Experimental Biology ; Wiley
Original Publication: [Bethesda, Md.] : The Federation, [c1987-
Ιατρικοί όροι (MeSH): Pulmonary Emphysema*/metabolism , Pulmonary Emphysema*/genetics , Pulmonary Emphysema*/pathology , Computational Biology*/methods , Idiopathic Pulmonary Fibrosis*/metabolism , Idiopathic Pulmonary Fibrosis*/genetics , Sialyltransferases*/metabolism , Sialyltransferases*/genetics , Pulmonary Fibrosis*/metabolism , Pulmonary Fibrosis*/genetics , Pulmonary Fibrosis*/pathology, Humans ; Animals ; Mice ; Transcriptome
Περίληψη: Emphysema and pulmonary fibrosis represent distinct patterns of chronic lung remodeling but may share molecular and cellular abnormalities. In this study, we analyzed public transcriptomic datasets of chronic obstructive pulmonary disease, emphysema, and idiopathic pulmonary fibrosis from the Gene Expression Omnibus database to explore shared disease-related signatures. Weighted gene co-expression network analysis and differential expression analysis were used to identify common molecular alterations, followed by functional enrichment, protein-protein interaction network construction, hub gene screening, immune infiltration analysis, transcription factor prediction, and single-cell RNA-sequencing validation. The integrated analysis revealed overlapping signatures related to cell adhesion, extracellular matrix organization, vascular regulation, immune responses, and epithelial homeostasis. Five hub genes were validated, and ST6GALNAC5 was further prioritized because of its association with sialylation and predominant enrichment in epithelial cells. Given that sialylation has been rarely investigated in pulmonary fibrosis and emphysema, we therefore further investigated ST6GALNAC5-related epithelial sialylation. Experimental validation on tissue samples showed reduced Sambucus nigra agglutinin lectin signals and decreased ST6GALNAC5 expression in lungs with coexisting emphysematous and fibrotic injury. In vitro experiments confirmed that ST6GALNAC5 overexpression attenuated bleomycin-induced epithelial cell injury. Together, these findings identify convergent molecular signatures across emphysematous and fibrotic lung diseases and suggest that impaired epithelial sialylation may represent a previously underappreciated feature of chronic lung remodeling.
(© 2026 Federation of American Societies for Experimental Biology.)
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Contributed Indexing: Keywords: ST6GALNAC5; bioinformatics analysis; emphysema; epithelial injury; idiopathic pulmonary fibrosis; sialylation
Substance Nomenclature: EC 2.4.99.- (Sialyltransferases)
Entry Date(s): Date Created: 20260915 Date Completed: 20260915 Latest Revision: 20260917
Update Code: 20260917
PubMed Central ID: PMC13576786
DOI: 10.1096/fj.202602975R
PMID: 42742537
Βάση Δεδομένων: MEDLINE
Περιγραφή
ISSN:1530-6860
DOI:10.1096/fj.202602975R