Metabolomic and proteomic analyses of primary Sjogren's syndrome.
Liquid chromatography-mass spectrometry
Metabolomics
Primary Sjogren’s syndrome
Proteomics
Journal
Immunobiology
ISSN: 1878-3279
Titre abrégé: Immunobiology
Pays: Netherlands
ID NLM: 8002742
Informations de publication
Date de publication:
09 2023
09 2023
Historique:
received:
30
05
2023
revised:
10
07
2023
accepted:
25
07
2023
medline:
29
8
2023
pubmed:
12
8
2023
entrez:
11
8
2023
Statut:
ppublish
Résumé
The pathogenesis of primary Sjogren's syndrome (pSS) has not been fully elucidated. We explored differentially expressed proteins and metabolic pathways in pSS using proteomics and metabolomics. 456 named proteins in total were identified, among which 50 were significantly changed in the pSS. Altered proteins were significantly associated with signaling pathways such as antigen processing and presentation, human immunodeficiency virus 1 infection, and FC gamma R-mediated phagocytosis. Meanwhile, 12 proteins, such as SH3BGRL3, TPM4, and CA1, can be used as potential clinical molecular markers. Moreover, 128 metabolites were significantly expressed in the pSS group. A total of 96 pathways were significantly enriched including central carbon metabolism in cancer, taurine and hypotaurine metabolism, and ABC transporters. Notably, both proteomics and metabolomics enriched glycolysis/gluconeogenesis metabolism, pentose phosphate pathway, and glutathione metabolism pathways. In this study, the progression mechanism of pSS was analyzed and novel biomarkers were identified by proteomics and metabolomics.
Identifiants
pubmed: 37567091
pii: S0171-2985(23)04524-2
doi: 10.1016/j.imbio.2023.152722
pii:
doi:
Substances chimiques
Biomarkers
0
SH3BGRL3 protein, human
0
Adaptor Proteins, Signal Transducing
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
152722Informations de copyright
Copyright © 2023 Elsevier GmbH. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.