Evidence map›Paper›PMID 42547464›Full record

ReviewAllergy, asthma & immunology research2026

Skin Lipid Dysregulation in Atopic Dermatitis and Related Inflammatory Skin Diseases.

Han Bi Kim, Jinseo Park, Chan Sol Lim, Ji Young Um, Bo Young Chung, Chun Wook Park, Dong-Kyu Lee, Hye One Kim

Abstract readReview
In one paragraph

Review in Allergy, asthma & immunology research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Han Bi KimDepartment of Dermatology, Hallym University Kangnam Sacred Heart Hospital, College of Medicine, Hallym University, Seoul, Korea.ORCID https://orcid.org/0000-0003-3190-7505
Jinseo ParkDepartment of Dermatology, Hallym University Kangnam Sacred Heart Hospital, College of Medicine, Hallym University, Seoul, Korea.ORCID https://orcid.org/0000-0003-2872-8215
Chan Sol LimDepartment of Dermatology, Hallym University Kangnam Sacred Heart Hospital, College of Medicine, Hallym University, Seoul, Korea.ORCID https://orcid.org/0009-0006-5627-0095
Ji Young UmDepartment of Dermatology, Hallym University Kangnam Sacred Heart Hospital, College of Medicine, Hallym University, Seoul, Korea.ORCID https://orcid.org/0000-0003-2044-199X
Bo Young ChungDepartment of Dermatology, Hallym University Kangnam Sacred Heart Hospital, College of Medicine, Hallym University, Seoul, Korea.ORCID https://orcid.org/0000-0002-2795-0140
Chun Wook ParkDepartment of Dermatology, Hallym University Kangnam Sacred Heart Hospital, College of Medicine, Hallym University, Seoul, Korea.ORCID https://orcid.org/0000-0003-4512-8668
Dong-Kyu LeeCollege of Pharmacy, Chung-Ang University, Seoul, Korea.ORCID https://orcid.org/0000-0003-2355-8560
Hye One KimDepartment of Dermatology, Hallym University Kangnam Sacred Heart Hospital, College of Medicine, Hallym University, Seoul, Korea. hyeonekim@gmail.com.ORCID https://orcid.org/0000-0001-5846-0008

Funding

Hallym UniversityMinistry of Health and Welfare RS-2023-KH141546National Research Foundation of Korea RS-2022-NR070251
6 · The paper itself

Abstract

Epidermal lipids are essential for skin barrier function and actively influence cutaneous immune homeostasis. Recent advances have transformed our understanding of skin lipid dysregulation in allergic diseases, revealing complex bidirectional relationships between barrier dysfunction and immune activation. This review provides a comprehensive analysis of the 2020-2025 literature on skin lipid metabolism in allergic and inflammatory diseases, with a particular focus on molecular mechanisms, diagnostic biomarkers, therapeutic advances, and implications for precision medicine. Key discoveries include the finding that sphingomyelin deacylase, long linked to ceramide (CER) deficiency, is actually the β-subunit of acid ceramidase. In atopic dermatitis, this enzyme shifts its substrate specificity to sphingomyelin, depleting the barrier lipid pool. Type 2 cytokines, particularly interleukin (IL)-4 and IL-13, suppress lipid biosynthesis through Janus kinase (JAK)/Signal Transducer and Activator of Transcription 6-mediated downregulation of fatty acid (FA) elongases. This suppression, particularly affecting elongation of very long-chain fatty acid (ELOVL) enzymes, such as ELOVL1, ELOVL3, and ELOVL6, disrupts the synthesis of ultra-long-chain CERs essential for barrier function. JAK inhibitors effectively reverse T helper 2 (Th2)-mediated lipid suppression, while optimized topical lipid ratios (3:1:1 CER: cholesterol: FA) enhance barrier repair. Innovations, such as lipid nanoparticles and microbiome-modulating therapies, further support personalized treatment strategies. The integration of barrier repair with targeted immunomodulation-guided by lipidomic and genomic profiling-marks a paradigm shift toward predictive and preventive approaches in allergic skin diseases. Early intervention strategies that simultaneously address immune dysregulation and lipid metabolism hold promise for preventing the atopic march and sustaining long-term remission.

Indexed as

acetyltransferasesacid ceramidaseallergic diseasesatopic dermatitisEpidermal lipidshypersensitivityinterleukinsprecision medicineskin

Identifiers

PMID42547464
PMCPMC13441561

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Registered trials

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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.