ArticleBiomedical engineering and computational biology2024
Uncovering the Therapeutic Target and Molecular Mechanism of Upadacitinib on Sjogren's Syndrome.
Article in Biomedical engineering and computational biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- The Th17/Treg axis: a key to understanding and treating autoimmune disorders.Open life sciences · 2026Article
- Sjögren's Syndrome: Epidemiology, Classification Criteria, Molecular Pathogenesis, Diagnosis, and Treatment.MedComm · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Upadacitinib, a selective Janus associated kinase 1 (JAK-1) inhibitor, can be prescribed particularly for the clinical treatment with Crohn's disease or rheumatoid arthritis. It is clinically observed that upadacitinib has been found with potential therapeutic effectiveness on Sjogren's syndrome (SS). However, the anti-SS targets and mechanisms involved in upadacitinib treatment remain uninvestigated. Materials and methods: Thus, this study was designed to identify therapeutic targets and mechanisms of upadacitinib for treating SS through conducting network pharmacology and molecular docking analyses. Results: In total, we identified 298 upadacitinib-related target genes, 1339 SS-related targets before collecting 56 overlapped target genes and 12 hub target genes. Upadacitinib largely exerted the critical biological processes including regulation of microenvironment homeostasis, inflammatory response, and cell apoptosis, and largely acted on pivotal molecular mechanisms including hypoxia-inducible factor 1 (HIF-1) signaling pathway, apoptosis pathway, phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway, or Th17 cell differentiation pathway. Molecular docking data suggested that upadacitinib exhibited the high affinities with signal transducer and activator of transcription 3 (STAT3), HIF1A, poly(ADP-ribose) polymerase 1 (PARP1) target proteins, in which the structural interactions between upadacitinib and STAT3, HIF1A, PARP1 showed potential therapeutic activities against SS. Conclusion: In conclusion, upadacitinib possesses the bright anti-inflammatory and anti-apoptotic activities on SS, and this study can provide a theoretical basis for clinical therapy of SS using upadacitinib.
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Registered trials
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