ArticleMedComm2026
Hemidesmosome Mutations Contribute to the Onset and Severity of Acquired Autoimmune Bullous Diseases.
Article in MedComm, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
20 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hemidesmosomes are structures that anchor junctions between basal epithelial cells and the basement membrane, essential for skin integrity. Genetic mutation of hemidesmosomes was well documented for the inherited bullous disorder, but is rarely investigated for acquired bullous disorders. We designed a 16-gene targeted capture panel and sequenced 202 patients with hemidesmosomes-related acquired disorders and 123 healthy controls, identifying 114 pathogenic variants in 15 genes, including 20.2% novel variants. Clinical relevance (disease severity and outcome) and immunohistochemistry results demonstrated that ITGA6, LAMC2, and EPPK1 mutations significantly affected the expression of hemidesmosome-related proteins, compared with controls with non-carriers. Functional studies in
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