ArticleInternational journal of molecular sciences2021
Increased Expression of 11β-Hydroxysteroid Dehydrogenase Type 1 Contributes to Epidermal Permeability Barrier Dysfunction in Aged Skin.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- A 11β-Hydroxysteroid Dehydrogenase Type 1 (11β-HSD1) Inhibitor, 11b-0048, Effectively Suppresses the Expression of 11β-HSD1 Activated in Cultured Keratinocytes and in Diabetic Murine Skin.Annals of dermatology · 2026Article
- Neurohormonal-Immune Dysregulation in Rosacea: Emerging Perspectives from the Skin-Gut-Brain Axis.Drug design, development and therapy · 2026Review
- Skin-Immune-Neuro-Gastro-Endocrine (SINGE) System: Lighting the Fire on Atopic Dermatitis Research.Dermatology practical & conceptual · 2025Review
- Hyperglycemia-activated 11β-hydroxysteroid dehydrogenase type 1 increases endoplasmic reticulum stress and skin barrier dysfunction.Scientific reports · 2023Article
- Treating Hypopituitarism in the Over 65s: Review of Clinical Studies.Clinical interventions in aging · 2023Review
- The link between cutaneous inflammation and cognitive impairment.Journal of the European Academy of Dermatology and Venereology : JEADV · 2022Review
- Transcriptome Analysis of Particulate Matter 2.5-Induced Abnormal Effects on Human Sebocytes.International journal of molecular sciences · 2022Article
- Synopsis of Barrier Function of Skin and Oral Mucosa-Volume 1.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Inactive cortisone is converted into active cortisol by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Excessive levels of active glucocorticoids could deteriorate skin barrier function; barrier impairment is also observed in aged skin. In this study, we aimed to determine whether permeability barrier impairment in the aged skin could be related to increased 11β-HSD1 expression. Aged humans (n = 10) showed increased cortisol in the stratum corneum (SC) and oral epithelium, compared to young subjects (n = 10). 11β-HSD1 expression (as assessed via immunohistochemical staining) was higher in the aged murine skin. Aged hairless mice (56-week-old, n = 5) manifested greater transepidermal water loss, lower SC hydration, and higher levels of serum inflammatory cytokines than the young mice (8-week-old, n = 5). Aged 11β-HSD1 knockout mice (n = 11), 11β-HSD1 inhibitor (INHI)-treated aged wild type (WT) mice (n = 5) and young WT mice (n = 10) exhibited reduced SC corticosterone level. Corneodesmosome density was low in WT aged mice (n = 5), but high in aged 11β-HSD1 knockout and aged INHI-treated WT mice. Aged mice exhibited lower SC lipid levels; this effect was reversed by INHI treatment. Therefore, upregulation of 11β-HSD1 in the aged skin increases the active-glucocorticoid levels; this suppresses SC lipid biosynthesis, leading to impaired epidermal permeability barrier.
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Registered trials
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