ArticleJournal of inflammation research2022
Multi-Transcriptomic Analysis and Experimental Validation Implicate a Central Role of STAT3 in Skin Barrier Dysfunction Induced Aggravation of Rosacea.
Article in Journal of inflammation research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Molecular Mechanisms in the Etiopathology of Rosacea-Systematic Review.International journal of molecular sciences · 2025Pooled it
- Immunomodulatory Effects of Poly-D,L-Lactic Acid on LL-37-Driven Rosacea-like Inflammation via Suppression of mTORC1 Signaling.International journal of molecular sciences · 2026Article
- Targeting skin barrier repair: mechanisms of action, therapeutic evidence, and clinical translation challenges of mesenchymal stem cell-derived exosomes.Stem cell research & therapy · 2026Review
- The exposomal imprint on rosacea: More than skin deep.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026Review
- Calcitonin gene-related peptide promotes mast cell-mediated neuroimmune inflammation through the CALCRL/RAMP1-JAK3-STAT1 axis in rosacea.Frontiers in immunology · 2026Article
- The role of skin barrier and immune abnormalities in the pathogenesis of Rosacea.Clinical and experimental medicine · 2025Review
- Impact of Rosacea on Keratinocyte Skin Cancers: A Prospective Case-Control Study of Basal and Squamous Cell Carcinoma Risk.Dermatology practical & conceptual · 2025Article
- Targeting Vascular and Inflammatory Crosstalk: Cannabigerol as a Dual-Pathway Modulator in Rosacea.International journal of molecular sciences · 2025Article
- Topographical variations in the skin barrier and their role in disease pathogenesis.Journal of the European Academy of Dermatology and Venereology : JEADV · 2025Review
- Niclosamide Alleviated Skin Inflammation and Restored the Balance between Effector and Regulatory T Cells in Skin.Biomolecules & therapeutics · 2025Article
- Keratin 6A promotes skin inflammation through JAK1-STAT3 activation in keratinocytes.Journal of biomedical science · 2025Article
- Targeting the STAT3/IL-36G signaling pathway can be a promising approach to treat rosacea.Journal of advanced research · 2025Article
- Bioinformatic analysis and experimental validation implicate STAT2-mediated angiogenic responses in rosacea pathogenesis.Archives of dermatological research · 2025Article
- Mechanisms and Recent Advances of Small-Molecule Therapeutics in Rosacea Treatment.Clinical, cosmetic and investigational dermatology · 2025Review
- A Case of Intense Pulsed Light Aggravated Rosacea Successfully Treated by Abrocitinib.Clinical, cosmetic and investigational dermatology · 2025Article
- Advances in the pathogenesis of rosacea.Frontiers in immunology · 2025Review
- Kushe Tincture Ameliorates DNCB-Induced Atopic Dermatitis by Affecting NF-Kb/JAK-STAT3 Pathway: Bioinformatics Analysis and Animal Experiment Verification.Journal of inflammation research · 2025Article
- The treatment of Tofacitinib for rosacea through the inhibition of the JAK/STAT signaling pathway.Archives of dermatological research · 2024Article
- Exploring the association between rosacea and acne by integrated bioinformatics analysis.Scientific reports · 2024Article
- Signaling pathways and targeted therapy for rosacea.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Rosacea is a chronic inflammatory skin disease with high morbidity. Previous studies have described the contribution of skin barrier dysfunction (SBD) in the progression of rosacea, but the specific mechanism remains unclear. In this study, we aim to investigate the key genes that may involve SBD-mediated rosacea aggravation. Methods: In this study, we evaluated the SBD patterns of rosacea based on the expression of 23 skin barrier-related genes (SBRGs) using a consensus clustering analysis, and revealed the SBD-mediated immune cells infiltration in rosacea using GSE65914 dataset. The key genes associated with SBD and rosacea progression were identified using WGCNA analysis and then verified in rosacea mice model. Results: Two distinct SBD patterns (moderate- and high-SBD patterns) were determined in rosacea. GO, KEGG and GSEA analysis revealed the differently immune-related signal pathways between two SBD patterns in rosacea. The XCell immune cell assays showed that the increased immune infiltration with SBD. Subsequently, the WGCNA analysis identified STAT3 as the hub gene related to rosacea and SBD, and correlation analysis revealed that STAT3 could contribute to the progression of rosacea partly by dysregulating immune infiltration via activating the cytokine/chemokines signal. Finally, the up-regulated STAT3 was verified in the epidermis of rosacea tissues and correlated with SBRGs expression using IHC and epidermal transcriptome data of rosacea. The vivo experiment showed that tape stripping-induced SBD evidently induced the expression of STAT3 and increased CD4 Conclusion: In conclusion, our results showed that the destruction of the skin barrier aggravates the inflammation levels and immune infiltration of rosacea partly by activating STAT3-mediated cytokine signal pathways in keratinocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.