Evidence map›Paper›PMID 42845230›Full record

ArticleAllergy, asthma & immunology research2026

Integrated RNA-Seq Profiling Identifies NRXN1+ Cell-Fibroblast Associated MAPK Signaling in Prurigo Nodularis.

Jiyun Jang, Young-Bok Lee, Hwee-Seon Park, Narang Hong, Hyung Don Kook, Hye Jung Jung, Jong-Il Kim, Jiyoung Ahn

Abstract read
In one paragraph

Article 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.

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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Jiyun Jang *Department of Biomedical Science, Seoul National University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0001-5145-334X
Young-Bok Lee *Department of Dermatology, College of Medicine, The Catholic University of Korea, Seoul, Korea.ORCID https://orcid.org/0000-0002-8642-2479
Hwee-Seon ParkDepartment of Biomedical Science, Seoul National University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0002-2649-3750
Narang HongDepartment of Dermatology, National Medical Center, Seoul, Korea.ORCID https://orcid.org/0000-0002-6542-4811
Hyung Don KookDepartment of Dermatology, National Medical Center, Seoul, Korea.ORCID https://orcid.org/0000-0001-6687-2125
Hye Jung JungDepartment of Dermatology, National Medical Center, Seoul, Korea.ORCID https://orcid.org/0000-0003-0995-5711
Jong-Il KimDepartment of Biomedical Science, Seoul National University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0002-7240-3744
Jiyoung AhnDepartment of Dermatology, National Medical Center, Seoul, Korea. jiyoung.ahn@nmc.or.kr.ORCID https://orcid.org/0000-0002-6766-9978

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposePrurigo nodularis (PN) is chronic pruritic dermatosis with hyperkeratotic nodules and persistent itch, occurring alone or with atopic dermatitis (AD). The molecular basis of nodular architecture and sustained pruritus remain poorly defined, particularly the role of fibroblasts and their interactions with neuronal components. This study aimed to identify PN-specific pathogenic profiles by comparing lesional transcriptomes from AD, atopic prurigo (AP), and PN.

methodsBulk RNA sequencing was performed on lesional skin from AD (n = 6), AP (n = 7), PN (n = 7), and healthy controls (HC; n = 4). Publicly available single-cell RNA-sequencing datasets were reanalyzed for cell-type signatures. Integrated analyses included differentially expressed genes, pathway enrichment, cell-type deconvolution, ligand-receptor inference, and immune cell profiling.

resultsPN lesions showed MAPK/ERK pathway enrichment in fibroblasts compared with AD and AP. NRXN1+ cells were inferred as major interacting partners of fibroblasts, with ligand-receptor interactions consistent with enhanced fibroblast MAPK/ERK activity. Immune pathway analyses showed weaker Th2 pathway activity in PN compared with AD/AP, providing context for neuronal-stromal interactions as a putative distinguishing feature.

conclusionsPN shows enhanced MAPK/ERK pathway enrichment in fibroblasts and inferred NRXN1+ cell-fibroblast interactions. This candidate axis may contribute to nodular lesion architecture and persistent pruritus, suggesting potential therapeutic strategies.

Indexed as

Atopic dermatitiscell communicationfibroblastsprurigoRNA-seqTh2 cells

Identifiers

PMID42845230
PMCPMC13655402

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