Evidence map›Paper›PMID 42338792›Full record

ArticleJID innovations : skin science from molecules to population health2026

Transcriptomic crossroads: Decoding genes and pathways that connect alopecia areata with chronic inflammatory skin disorders.

Hadis Abdolahzadeh, Sabrina Henne, Amir Mokhlesi, Jörg Wenzel, Stefanie Heilmann-Heimbach, Regina C Betz, F Buket Basmanav

Abstract read
In one paragraph

Article in JID innovations : skin science from molecules to population health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

7 authors.

Hadis AbdolahzadehInstitute of Human Genetics, School of Medicine, University Hospital Bonn, University of Bonn, Bonn, Germany.
Sabrina HenneInstitute of Human Genetics, School of Medicine, University Hospital Bonn, University of Bonn, Bonn, Germany.
Amir MokhlesiDepartment of Animal Sciences and Marine Biology, Faculty of Life Sciences and Biotechnology, Shahid Beheshti University, Tehran, Iran.
Jörg WenzelDepartment of Dermatology and Allergy, University Hospital Bonn, Bonn, Germany.
Stefanie Heilmann-HeimbachInstitute of Human Genetics, School of Medicine, University Hospital Bonn, University of Bonn, Bonn, Germany.
Regina C BetzInstitute of Human Genetics, School of Medicine, University Hospital Bonn, University of Bonn, Bonn, Germany.
F Buket BasmanavInstitute of Human Genetics, School of Medicine, University Hospital Bonn, University of Bonn, Bonn, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alopecia areata (AA) is an immune-mediated hair loss disorder that frequently co-occurs with chronic inflammatory skin disorders, such as atopic dermatitis, vitiligo, and psoriasis. Emerging evidence suggest that such comorbidity profiles represent clinical AA subtypes with distinct etiological underpinnings. However, mechanistic insights remain limited owing to a lack of molecular datasets from comorbid patient cohorts. In this study, we addressed this gap by leveraging publicly available case-control gene expression datasets from AA, atopic dermatitis, vitiligo, and psoriasis for an integrative analysis. Our results revealed a statistically significant overlap between gene expression signatures of AA and each chronic inflammatory skin disorder, suggesting that their co-occurrence is not coincidental. Downstream analyses of shared gene expression signatures suggested catecholamine signaling and hair/skin-pigmentation-related processes as possible drivers of AA and vitiligo codevelopment, whereas skin barrier defects and dysregulation of specific immune response pathways may underlie the comorbid development of AA with atopic dermatitis or psoriasis. This study provides a foundation for future mechanistic investigations into skin, hair follicle, and immune system interactions that drive distinct comorbid AA subtypes.

Indexed as

Alopecia areataAtopic dermatitisGene expressionPsoriasisVitiligo

Identifiers

PMID42338792
PMCPMC13285374

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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.