ArticleJournal of inflammation research2026
SIRT6 Aggravates Psoriasiform Skin Inflammation Through Modulation of the SOCS2-STAT1/3 Pathway.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: To investigate the role and molecular mechanisms of the deacetylase SIRT6 in psoriasis and evaluate its potential as a therapeutic target for topical treatment. Methods: The expression of SIRT6 in psoriatic lesions and healthy skin was analyzed using datasets from the GEO database. In vitro, Human Immortalized Epidermal Cells (HaCaT) were stimulated with TNF-α to establish a psoriasis-like cellular model. SIRT6 was overexpressed or knocked down in HaCaT cells to evaluate its effects on keratinocyte inflammation, proliferation, and migration. Integrated transcriptomic analysis and subsequent validation were conducted to explore the signaling pathways regulated by SIRT6. Changes in mRNA expression, protein levels and inflammatory cytokine secretion were assessed by RT-qPCR, Western blotting, immunohistochemistry, and ELISA. Therapeutic potential was assessed using a SIRT6 inhibitor-loaded alginate/carbomer hydrogel in an imiquimod-induced psoriasiform dermatitis mouse model and in human psoriatic skin explants ex vivo. Results: GEO dataset analysis revealed that SIRT6 expression was significantly higher in psoriatic lesions than in either healthy controls or non-lesional skin (both Conclusion: SIRT6 exacerbates psoriasiform inflammation by modulating the SOCS2-STAT1/3 signaling pathway. These findings suggest that topical inhibition of SIRT6 may represent a potential therapeutic strategy for psoriasis.
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