ReviewInternational journal of molecular sciences2016
Molecular Mechanisms of Cutaneous Inflammatory Disorder: Atopic Dermatitis.
Review in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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
50 citing papers in PubMed, 141 citations in OpenAlex.
- Berberine Inhibits Eczematous SkinInternational journal of molecular sciences · 2026Article
- Epithelial-Dermal Immune Memory: TrackingInternational journal of molecular sciences · 2026Review
- Exploring Cyclo (-Gly-Pro) for inflammation modulation in atopic dermatitis: a study on streptococcal postbiotics.Genes & genomics · 2026Article
- Phosphatidylserine liposomes containing metformin mitigate experimental atopic dermatitis: evidence for Akt/mTOR pathway involvement.Inflammopharmacology · 2026Article
- The Intervention Effect of Externally Applying or Orally AdministeringMicroorganisms · 2026Article
- Unlocking the molecular pathway of atopic dermatitis: journey so far and roads ahead.Inflammopharmacology · 2025Review
- Review
- Efficacy of acupoint injection in the treatment of chronic eczema and its influence on peripheral blood T cells.World journal of clinical cases · 2024Article
- Antioxidant, Antibacterial Properties of Novel Peptide CP by Enzymatic Hydrolysis ofMarine drugs · 2024Article
- Potential Indications of Dupilumab in Th-2 Inflammatory Disease.Reviews on recent clinical trials · 2024Review
- Sp1-mediated miR-193b suppresses atopic dermatitis by regulating HMGB1.The Kaohsiung journal of medical sciences · 2023Article
- Construction and verification of atopic dermatitis diagnostic model based on pyroptosis related biological markers using machine learning methods.BMC medical genomics · 2023Article
- Exosomes with overexpressed miR 147a suppress angiogenesis and infammatory injury in an experimental model of atopic dermatitis.Scientific reports · 2023Article
- Matrine regulates Th1/Th2 inflammatory responses by inhibiting the Hsp90/NF-κB signaling axis to alleviate atopic dermatitis.The Kaohsiung journal of medical sciences · 2023Article
- Interactions betweenInternational journal of molecular sciences · 2023Article
- Increased Expression of Toll-Like Receptor (TLR) 2 and TLR6 on Peripheral Blood Monocytes by Induction of Staphylococcal Enterotoxin B During Exacerbation of Atopic Dermatitis Patients.Clinical, cosmetic and investigational dermatology · 2023Article
- Hydrolyzable Tannins in the Management of Th1, Th2 and Th17 Inflammatory-Related Diseases.Molecules (Basel, Switzerland) · 2022Review
- Sargassum horneri extract containing polyphenol alleviates DNCB-induced atopic dermatitis in NC/Nga mice through restoring skin barrier function.Histology and histopathology · 2022Article
- Unveiling the Ability of Witch Hazel (International journal of molecular sciences · 2022Article
- Saikosaponin A and Saikosaponin C Reduce TNF-α-Induced TSLP Expression through Inhibition of MAPK-Mediated EGR1 Expression in HaCaT Keratinocytes.International journal of molecular sciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atopic dermatitis (AD) is a multifactorial inflammatory skin disease resulting from interactions between genetic susceptibility and environmental factors. The pathogenesis of AD is poorly understood, and the treatment of recalcitrant AD is still challenging. There is accumulating evidence for new gene polymorphisms related to the epidermal barrier function and innate and adaptive immunity in patients with AD. Newly-found T cells and dendritic cell subsets, cytokines, chemokines and signaling pathways have extended our understanding of the molecular pathomechanism underlying AD. Genetic changes caused by environmental factors have been shown to contribute to the pathogenesis of AD. We herein present a review of the genetics, epigenetics, barrier dysfunction and immunological abnormalities in AD with a focus on updated molecular biology.
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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.