ArticleInternational journal of molecular sciences2022
Transcriptomic Profiling of Peripheral Edge of Lesions to Elucidate the Pathogenesis of Psoriasis Vulgaris.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Luteolin Disrupts Keratinocyte-Dendritic Cell Communication in Psoriasis by Targeting Rh Family C Glycoprotein.Mediators of inflammation · 2026Article
- IL-17C as a Driver of Inflammation in Psoriasis.Advances in therapy · 2025Review
- Emerging Roles of Ferroptosis in Skin Pathophysiology.The Journal of investigative dermatology · 2025Review
- ACSS2 and metabolic diseases: from lipid metabolism to therapeutic target.Lipids in health and disease · 2025Review
- Tanshinone I Ameliorates Psoriasis-Like Dermatitis by Suppressing Inflammation and Regulating Keratinocyte Differentiation.Drug design, development and therapy · 2025Article
- Ferroptosis of select skin epithelial cells initiates and maintains chronic systemic immune-mediated psoriatic disease.The Journal of clinical investigation · 2024Article
- Elucidating the NB-UVB mechanism by comparing transcriptome alteration on the edge and center of psoriatic plaques.Scientific reports · 2023Article
- Crosstalk: keratinocytes and immune cells in psoriasis.Frontiers in immunology · 2023Review
- Revisiting the interleukin 17 family of cytokines in psoriasis: pathogenesis and potential targets for innovative therapies.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Elucidating transcriptome in the peripheral edge of the lesional (PE) skin could provide a better understanding of the molecules or signalings that intensify inflammation in the PE skin. Full-thickness biopsies of PE skin and uninvolved (UN) skin were obtained from psoriasis patients for RNA-seq. Several potential differentially expressed genes (DEGs) in the PE skin compared to those in the UN skin were identified. These DEGs enhanced functions such as angiogenesis, growth of epithelial tissue, chemotaxis and homing of cells, growth of connective tissues, and degranulation of myeloid cells beneath the PE skin. Moreover, the canonical pathways of IL-17A, IL-6, and IL-22 signaling were enriched by the DEGs. Finally, we proposed that inflammation in the PE skin might be driven by the IL-36/TLR9 axis or IL-6/Th17 axis and potentiated by IL-36α, IL-36γ, IL-17C, IL-8, S100A7, S100A8, S100A9, S100A15, SERPINB4, and hBD-2. Along with IL-36α, IL-17C, and IκBζ, ROCK2 could be an equally important factor in the pathogenesis of psoriasis, which may involve self-sustaining circuits between innate and adaptive immune responses via regulation of IL-36α and IL-36γ expression. Our finding provides new insight into signaling pathways in PE skin, which could lead to the discovery of new psoriasis targets.
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Registered trials
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