ArticleMediators of inflammation2025
Inhibition of SIK1 Alleviates the Pathologies of Psoriasis by Disrupting IL-17 Signaling.
Article in Mediators of inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- SIK inhibitor HG-9-91-01 suppresses the pathogenic activity of fibroblast-like synoviocytes in rheumatoid arthritis.RMD open · 2026Article
- The multifaceted role of NF-κB signaling in psoriasis: from inflammatory amplification to epidermal remodeling.Frontiers in immunology · 2026Review
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Authors and funding
7 authors.
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Abstract
Psoriasis is an inflammatory skin disease mediated by multiple immune cells, including T cells, macrophages, and dendritic cells, which exhibit complex pathologies and limited clinical treatment. Here, we found that salt-inducible kinase 1 (SIK1) was upregulated in the imiquimod (IMQ)-induced psoriasis mouse model. This increment may be due to a higher level of interleukin-17, which promoted the expression of SIK1 in keratinocytes. Inhibition of SIK1 kinase activity using a small molecular inhibitor (HG-9-91-01 or YKL-06-062) dramatically alleviated IMQ-induced psoriasis, showing reduced epidermal thickness, inflammation, and hyperproliferative epidermal keratinocytes. Our data demonstrated that SIK1 inhibitors HG-9-91-01 or YKL-06-062 blocked the expression of IL-17-induced proinflammatory cytokines and chemokines, including
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