Evidence map›Paper›PMID 41676306›Full record

ArticleAmerican journal of translational research2026

Dihydroartemisinin attenuates pemphigus vulgaris by regulating Dsg3 and the TLR9/NF-κB pathway.

Yu Cui, Shuxia Song, Yi Cheng, Caixia Hu, Molin Yang, Wenqing Wang

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Article in American journal of translational 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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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.

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Yu CuiDepartment of Dermatology, The Fourth Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Shuxia SongDepartment of Immunology, Hebei Medical University Shijiazhuang, Hebei, China.
Yi ChengDepartment of Dermatology, The Fourth Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Caixia HuDepartment of Dermatology, The Fourth Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Molin YangDepartment of Dermatology, The Fourth Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Wenqing WangDepartment of Dermatology, The Fourth Hospital of Hebei Medical University Shijiazhuang, Hebei, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo evaluate the therapeutic efficacy of dihydroartemisinin (DHA) in pemphigus vulgaris (PV).

methodsBased on network pharmacology analysis, the TLR9/NF-κB signaling axis was selected as the primary pathway of interest. Skin specimens were first validated using immunohistochemistry. Subsequently, HaCaT cells were incubated. Desmoglein 3 (Dsg3) expression was detected using immunofluorescence staining. Cell viability was evaluated using MTS assay. The expression levels of TLR9, TRAF6, MyD88, p-NF-κB p65, MMP-9, and ADAM10 in HaCaT cells treated with control IgG (C-IgG), PV-IgG, and DHA were then examined by western blotting. Finally, these indicators were evaluated in Kunming mice. The results demonstrated that DHA suppressed PV-IgG - induced Dsg3 internalization and depletion. PV-IgG appeared to activate the NF-κB pathway through TLR9/TRAF6 signaling, while DHA effectively inhibited this effect. Moreover, DHA downregulated the expression of ADAM10 and MMP-9, critical proteases involved in the pathogenesis of PV.

Indexed as

ADAM10dihydroartemisininDsg3MMP-9network pharmacologyPemphigus vulgarisp-NF-κB p65TLR9TRAF6

Identifiers

PMID41676306
PMCPMC12886154

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