ArticleThe Journal of investigative dermatology2017
Alterations in Epidermal Eicosanoid Metabolism Contribute to Inflammation and Impaired Late Differentiation in FLG-Mutated Atopic Dermatitis.
Article in The Journal of investigative dermatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 53 citations in OpenAlex.
- PPARα deficiency causes skin dysbiosis and triggers innate immunity in keratinocytes.Cell death & disease · 2026Article
- Research Progress on Construction Technology of 3D Human Skin Models and Its Application Prospects in Dermatology.International journal of molecular sciences · 2026Review
- Mimicking the LOX-Related Autosomal Recessive Congenital Ichthyosis Skin Disease Using a CRISPR-Cas9 System and Unravelling 12S-LOX Function in the Skin.Dermatopathology (Basel, Switzerland) · 2025Article
- Unlocking the molecular pathway of atopic dermatitis: journey so far and roads ahead.Inflammopharmacology · 2025Review
- Characterization of Inflammatory Mediators and Metabolome in Interstitial Fluid Collected with Dermal Open Flow Microperfusion before and at the End of Dupilumab Treatment in Atopic Dermatitis.Journal of proteome research · 2024Article
- Exploring the Metabolic Effects of a Herbal Remedy ofAntioxidants (Basel, Switzerland) · 2024Article
- Skin Barrier- and Immune Response-Related Biomarkers of Solar UVR Exposure Comparing Indoor and Outdoor Workers.JID innovations : skin science from molecules to population health · 2024Article
- Effects of donkey milk on UVB-induced skin barrier damage and melanin pigmentation: A network pharmacology and experimental validation study.Frontiers in nutrition · 2023Article
- Transcriptomic Analysis of the Major Orphan Ichthyosis Subtypes Reveals Shared Immune and Barrier Signatures.The Journal of investigative dermatology · 2022Article
- Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis.JID innovations : skin science from molecules to population health · 2022Review
- An Overview of the Latest Metabolomics Studies on Atopic Eczema with New Directions for Study.International journal of molecular sciences · 2022Review
- Small, Cationic Antifungal Proteins from Filamentous Fungi InhibitMicrobiology spectrum · 2022Article
- Holistic health record for Hidradenitis suppurativa patients.Scientific reports · 2022Article
- Revisiting the Roles of Filaggrin in Atopic Dermatitis.International journal of molecular sciences · 2022Review
- Atopic Dermatitis: The Fate of the Fat.International journal of molecular sciences · 2022Review
- Bioengineered Efficacy Models of Skin Disease: Advances in the Last 10 Years.Pharmaceutics · 2022Review
- Arachidonate 15-lipoxygenase type B: Regulation, function, and its role in pathophysiology.Frontiers in pharmacology · 2022Review
- Analysis of the gut microbiome to validate a mouse model of pellagra.Bioscience of microbiota, food and health · 2022Article
- Synergistic Effects of Korean Red Ginseng Extract and the Conventional Systemic Therapeutics of Atopic Dermatitis in a Murine Model.Nutrients · 2021Article
- Update on the Pathogenesis and Therapy of Atopic Dermatitis.Clinical reviews in allergy & immunology · 2021Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 4 countries.
Funding
Abstract
Loss-of-function mutations in the FLG gene cause ichthyosis vulgaris (IV) and represent the major predisposing genetic risk factor for atopic dermatitis (AD). Although both conditions are characterized by epidermal barrier impairment, AD also exhibits signs of inflammation. This work was aimed at delineating the role of FLG loss-of-function mutations on eicosanoid metabolism in IV and AD. Using human epidermal equivalents (HEEs) generated with keratinocytes isolated from nonlesional skin of patients with FLG wild-type AD (WT/WT), FLG-mutated AD (FLG/WT), IV (FLG/FLG), or FLG WT control skin, we assessed the potential autocrine role of epidermal-derived eicosanoids in FLG-associated versus FLG-WT AD pathogenesis. Ultrastructural analyses demonstrated abnormal stratum corneum lipid architecture in AD and IV HEEs, independent of FLG genotype. Both AD (FLG/WT) and IV (FLG/FLG) HEEs showed impaired late epidermal differentiation. Only AD (FLG/WT) HEEs exhibited significantly increased levels of inflammatory cytokines. Analyses of lipid mediators revealed increased arachidonic acid and 12-lipoxygenase metabolites. Whereas treatment of control HEEs with arachidonic acid increased expression of inflammatory cytokines, 12-hydroxy-eicosatetraenoic acid attenuated expression of late differentiation markers. Thus, FLG mutations lead to alterations in epidermal eicosanoid metabolism that could serve as an autocrine trigger of inflammation and impaired late epidermal differentiation in AD.
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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 OpenQuestion graph.