Research progress on multi-omics biomarkers in Sjogren's syndrome.
- Author:
Xueqin ZHOU
1
;
Huan LI
2
;
Zhina ZHAO
2
;
Qin LI
2
;
Bingsen WANG
3
;
Songwei LI
4
Author Information
1. First Clinical Medical College, Henan University of Chinese Medicine, Zhengzhou 450046, China.
2. Department of Rheumatology, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450099, China.
3. Department of Immunology, Henan Province Hospital of Traditional Chinese Medicine, Zhengzhou 450053, China.
4. Department of Rheumatology, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450099, China. *Corresponding author, E-mail: ryanzzdx@yeah.net.
- Publication Type:English Abstract
- MeSH:
Humans;
Sjogren's Syndrome/diagnosis*;
Biomarkers/analysis*;
Metabolomics/methods*;
Proteomics/methods*;
Genomics;
Multiomics
- From:
Chinese Journal of Cellular and Molecular Immunology
2025;41(10):921-928
- CountryChina
- Language:Chinese
-
Abstract:
Sjogren's syndrome (SS) is a common autoimmune disorder that primarily targets exocrine glands, leading to hallmark manifestations of xerostomia and xerophthalmia, with potential progression to multisystem involvement. The rapid advances in omics technologies-including metabolomics, proteomics, and transcriptomics-have yielded substantial insights into SS pathophysiology. This review consolidates current evidence on omics-derived biomarkers in SS. Studies consistently implicate aberrant glucose metabolism, neutrophil-derived enzyme activity, mitochondrial bioenergetic impairment, ferroptosis, and apoptotic pathways as central to SS development. These findings refine our understanding of disease mechanisms and the heterogeneity of therapeutic responses. Hydroxyproline has emerged as a candidate marker for distinguishing SS from IgG4-related disease, whereas distinct cytokine and chemokine signatures may enable earlier diagnosis. Genomic analyses demonstrate a robust association between expression of the rs11797 locus and SS-related lymphomagenesis, and several genes controlling DNA methylation represent promising therapeutic targets. Collectively, these findings lay the groundwork for personalized risk stratification and intervention in SS. The review concludes by summarizing existing progress and outlining priorities for future omics-based investigations.
