ArticleThe Journal of investigative dermatology2015
Decreased Expression of Caveolin-1 Contributes to the Pathogenesis of Psoriasiform Dermatitis in Mice.
Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Macrophage INSIG1 deficiency drives psoriasiform dermatitis via the SREBP2-STAT1 axis.Nature communications · 2026Article
- SLURP2 Enlarges Adipocytes and Induces IL-23-Producing Macrophages in Murine Dermal Adipose Tissue.Experimental dermatology · 2026Article
- The invisible agitators: exploring the viral interplay in psoriatic immune dysregulation.Immunologic research · 2025Review
- Scaffolds with spatiotemporally controlled growth factor delivery and cyclodextrin-enabled antagonism of growth factor receptor sequestration promote cutaneous wound healing.NPJ Regenerative medicine · 2025Article
- A water-soluble caveolin-1 peptide inhibits psoriasis-like skin inflammation by suppressing cytokine production and angiogenesis.Scientific reports · 2024Article
- Downregulation of Caveolae-Associated Proteins in Psoriasis: A Case Series Study.JID innovations : skin science from molecules to population health · 2024Article
- Interactive mechanisms between caveolin-1 and actin filaments or vimentin intermediate filaments instruct cell mechanosensing and migration.Journal of molecular cell biology · 2023Article
- Caveolae Mechanotransduction at the Interface between Cytoskeleton and Extracellular Matrix.Cells · 2023Review
- Involvement of caveolin-1 in skin diseases.Frontiers in immunology · 2022Review
- Type I interferon activation and endothelial dysfunction in caveolin-1 insufficiency-associated pulmonary arterial hypertension.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Acitretin Promotes the Differentiation of Myeloid-Derived Suppressor Cells in the Treatment of Psoriasis.Frontiers in medicine · 2021Article
- Caveolin-1 as a possible target in the treatment for acne.Experimental dermatology · 2020Review
- Caveolin as a Universal Target in Dermatology.International journal of molecular sciences · 2019Review
- Caveolin-1 in skin aging - From innocent bystander to major contributor.Ageing research reviews · 2019Review
- Downregulated Caveolin-1 expression in circulating monocytes may contribute to the pathogenesis of psoriasis.Scientific reports · 2019Article
- Caveolin-1 as a pathophysiological factor and target in psoriasis.NPJ aging and mechanisms of disease · 2019Review
- The autophagic degradation of Cav-1 contributes to PA-induced apoptosis and inflammation of astrocytes.Cell death & disease · 2018Article
- Caveolin-1-Knockout Mouse as a Model of Inflammatory Diseases.Journal of immunology research · 2018Article
- Epidermal CD147 expression plays a key role in IL-22-induced psoriatic dermatitis.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psoriasis is a chronic inflammatory skin disease characterized by excessive proliferation and abnormal keratinocyte development, in which T helper type 17 cells and signal transducer and activator of transcription 3 (STAT3) activation have pivotal roles. Moreover, caveolin-1 (CAV-1) has been implicated in the regulation of signal transduction, and aberrant CAV-1 expression is involved in a variety of diseases. However, whether CAV-1 is involved in psoriasis is unknown. Here we examined CAV-1 expression in the psoriatic epidermis and investigated its role in the pathogenesis of psoriasis. CAV-1 was markedly reduced in lesional epidermis of psoriasis patients. CAV1 silencing in keratinocytes in vitro revealed significant activation of STAT3, leading to increased expression of keratin 16 and several cytokine/chemokines, such as IL-6, C-X-C chemokine ligand 8 (CXCL8), CXCL9, and C-C chemokine ligand 20. In addition, psoriasis-related cytokines, including tumor necrosis factor-α (TNF-α), decreased CAV-1 expression in keratinocytes. Finally, administration of CAV-1 scaffolding domain peptide in a murine model of psoriasis-like skin inflammation induced by imiquimod improved the skin phenotype and reduced epidermal thickness and infiltrating cell counts. Furthermore, expression of TNF-α, IL-17A, and IL-23 was significantly suppressed by this treatment. Collectively, our study indicated that CAV-1 participates in the pathogenesis of psoriasis by regulating the STAT3 pathway and cytokine networks.
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