ReviewInternational journal of molecular sciences2020
Regulation of Filaggrin, Loricrin, and Involucrin by IL-4, IL-13, IL-17A, IL-22, AHR, and NRF2: Pathogenic Implications in Atopic Dermatitis.
Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 226 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
226 citing papers in PubMed, 3 syntheses or guidelines pooled it, 365 citations in OpenAlex.
- The genetic basis of dermatophytosis skin infection susceptibility.Nature communications · 2026Pooled it
- Age differences in psychological comorbidity in atopic dermatitis: a systematic review and meta-analysis.Frontiers in public health · 2026Pooled it
- Pooled it
- A Novel Multi-Component Formulation Reduces Inflammation In Vitro and Clinically Lessens the Symptoms of Chronic Eczematous Skin.International journal of molecular sciences · 2023Trial
- Ameliorative effects ofMolecular medicine reports · 2026Article
- Long-Term Human Skin Platform for Modeling Chronic Inflammation, Environmental Stress, and Therapeutic Intervention.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A Subcellular Keap1-Nrf2 Disruption Strategy for Atopic Dermatitis Therapy.Journal of medicinal chemistry · 2026Article
- Article
- Rethinking Head and Neck Atopic Dermatitis: Pathogenic Axes and Emerging Therapeutic Directions.American journal of clinical dermatology · 2026Review
- IL-1 family signalling drives mucosal defence against systemic Candida albicans infection.Nature microbiology · 2026Article
- From Barrier Disruption and Immune Dysregulation to Targeted Therapies in Atopic Dermatitis.Clinical reviews in allergy & immunology · 2026Review
- Advancing Epidermal Barrier Resilience in Atopic Dermatitis with Isosorbide Di-Fatty Acid Esters: From Disruption to Restoration.Biomolecules · 2026Review
- Potential Supportive Effects of AP Collagen Peptides on Skin Hydration in a Mouse Model of Oxazolone-Induced Atopic Dermatitis.Journal of microbiology and biotechnology · 2026Article
- Pink lotus flower (Biomedical reports · 2026Article
- Translational Assessment of a Cell-Penetrating Peptide Topical Formulation for Repairing Barrier Dysfunction in Human Skin.International journal of molecular sciences · 2026Article
- The JAK-STAT pathway in allergic diseases: from pathogenesis to targeted therapy.Biomarker research · 2026Review
- Commensal yeast Malassezia produces tryptophan metabolites to promote tissue homeostasis via the aryl hydrocarbon receptor in mice.Nature microbiology · 2026Article
- Oral Administration ofAnimals : an open access journal from MDPI · 2026Article
- Review
- Critical role of keratinocytes and protease-activated receptor 2 in secondary lymphedema development.Clinical and translational medicine · 2026Article
166 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Atopic dermatitis (AD) is an eczematous, pruritic skin disorder with extensive barrier dysfunction and elevated interleukin (IL)-4 and IL-13 signatures. The barrier dysfunction correlates with the downregulation of barrier-related molecules such as filaggrin (FLG), loricrin (LOR), and involucrin (IVL). IL-4 and IL-13 potently inhibit the expression of these molecules by activating signal transducer and activator of transcription (STAT)6 and STAT3. In addition to IL-4 and IL-13, IL-22 and IL-17A are probably involved in the barrier dysfunction by inhibiting the expression of these barrier-related molecules. In contrast, natural or medicinal ligands for aryl hydrocarbon receptor (AHR) are potent upregulators of FLG, LOR, and IVL expression. As IL-4, IL-13, IL-22, and IL-17A are all capable of inducing oxidative stress, antioxidative AHR agonists such as coal tar, glyteer, and tapinarof exert particular therapeutic efficacy for AD. These antioxidative AHR ligands are known to activate an antioxidative transcription factor, nuclear factor E2-related factor 2 (NRF2). This article focuses on the mechanisms by which FLG, LOR, and IVL expression is regulated by IL-4, IL-13, IL-22, and IL-17A. The author also summarizes how AHR and NRF2 dual activators exert their beneficial effects in the treatment of AD.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.