ArticleCell death & disease2021
MiR-193b-3p-ERBB4 axis regulates psoriasis pathogenesis via modulating cellular proliferation and inflammatory-mediator production of keratinocytes.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- MiR-146b-5p/ERBB4 Axis Drives LPS-induced Acute Kidney Injury by Modulating NF-κB/p65.Biochemical genetics · 2026Article
- Dental pulp stem cell-derived exosomes attenuate psoriatic inflammation by restoring epithelial redox homeostasis via a miR-1246/miR-17-3p-GPX2-NF-κB axis.Stem cell research & therapy · 2026Article
- Updates on the role of miR-193b in the pathogenesis of human cancers and other diseases.Biochemistry and biophysics reports · 2026Review
- Evaluation of 3D biomimetic microcarriers for enhancing therapeutic efficacy of human umbilical cord mesenchymal stem cells in psoriasis treatment.Frontiers in immunology · 2026Article
- Regulatory role of POSTN in keloid pathogenesis.Molecular medicine reports · 2025Article
- YAP1 facilitates the pathogenesis of psoriasis via modulating keratinocyte proliferation and inflammation.Cell death & disease · 2025Article
- Inflammatory memory-activated biomimetic nanovesicles regulate neutrophil plasticity and metabolic reprogramming for rapid diabetic wound healing via targeting miR-193a-5p/TLR4/JNK/P38 MAPK pathways.Journal of nanobiotechnology · 2025Article
- Synaptotagmin-1 attenuates myocardial programmed necrosis and ischemia/reperfusion injury through the mitochondrial pathway.Cell death & disease · 2025Article
- Recent progress on DNA methylation in psoriasis.Frontiers in genetics · 2025Review
- Recent advances on Hippo-YAP pathway in skin diseases.Frontiers in immunology · 2025Review
- Article
- RNA-Based Antipsoriatic Gene Therapy: An Updated Review Focusing on Evidence from Animal Models.Drug design, development and therapy · 2024Review
- Necessary and sufficient factors of keratinocytes in psoriatic dermatitis.Frontiers in immunology · 2024Article
- Article
- The exosomal secretomes of mesenchymal stem cells extracted via 3D-printed lithium-doped calcium silicate scaffolds promote osteochondral regeneration.Materials today. Bio · 2023Article
- Sp1-mediated miR-193b suppresses atopic dermatitis by regulating HMGB1.The Kaohsiung journal of medical sciences · 2023Article
- Review
- MiR-125a-3p alleviates hyperproliferation of keratinocytes and psoriasis-like inflammation by targeting TLR4/NF-κB pathway.Postepy dermatologii i alergologii · 2023Article
- The critical importance of epigenetics in autoimmune-related skin diseases.Frontiers of medicine · 2023Review
- Identification of Chemokines-Related miRNAs as Potential Biomarkers in Psoriasis Based on Integrated Bioinformatics Analysis.Combinatorial chemistry & high throughput screening · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 2 institutions in 2 countries.
Funding
Abstract
Psoriasis is an auto-inflammatory skin disease characterized by abnormal activation of epidermal keratinocytes, aberrant neovascularization, and dysregulation of immune cells. MicroRNAs are small non-coding RNAs that mainly function in the post-transcriptional regulation of gene expression. Recently, accumulating evidence has demonstrated that expression of microRNAs is dysregulated in psoriasis patients and microRNAs play key roles in psoriasis pathogenesis. Downregulation of miR-193b-3p has been identified to be associated with psoriasis development. However, the precise functions and action mechanisms of miR-193b-3p in psoriasis pathogenesis remain unclear. In this study, we confirmed the downregulation of miR-193b-3p in psoriasis patients, psoriasis-like inflammatory cellular models, and an imiquimod (IMQ) -induced mouse model. A negative correlation was found between miR-193b-3p level and patient Psoriasis Area and Severity Index (PASI) score. Furthermore, miR-193b-3p suppressed proliferation, inflammatory-factor secretion, and the STAT3 and NF-κB signaling pathways in keratinocytes. Importantly, intradermal injection of agomiR-193b-3p blocked, whereas antagomiR-193b-3p augmented, the psoriasis-like inflammation in the IMQ-induced mouse model. Bioinformatics analysis and the dual-luciferase reporter assay showed that miR-193b-3p targets ERBB4 3' untranslated region (UTR). In addition, ERBB4 induced proliferation, inflammatory-factor production, and the STAT3 and NF-κB pathways in keratinocytes. Most importantly, forced expression of ERBB4 could attenuate the effects of miR-193b-3p in keratinocytes, indicating that miR-193b-3p inhibits keratinocyte activation by directly targeting ERBB4. In conclusion, our findings demonstrated that the miR-193b-3p-ERBB4 axis underlies the hyperproliferation and aberrant inflammatory-factor secretion of psoriatic keratinocytes, providing a novel, microRNA-related causal mechanism and a potential therapeutic target in psoriasis.
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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.