ArticleSkin health and disease2026
Targeting ST18-mediated pathomechanism in pemphigus vulgaris through voltage-dependent anion channel inhibition.
Article in Skin health and disease, 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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14 authors.
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Abstract
Background: Pemphigus vulgaris (PV), a severe mucocutaneous blistering disease, results from autoantibody-mediated destabilization of epidermal cell-cell adhesion. A functional risk variant at the ST18 locus was found to promote epidermal ST18 expression. Increased ST18 expression was found to aggravate the deleterious effect of PV autoantibodies in part through induction of p53-mediated proapoptotic pathways. The voltage-dependent anion channel (VDAC) is a key regulator of mitochondria-mediated apoptosis. Objectives: To delineate the interplay between ST18 and VDAC in apoptosis regulation, and the therapeutic potential of VDAC inhibitors in PV. Methods: We used global RNA sequencing (RNAseq) of human keratinocytes to assess ST18-dependent changes in Results: Keratinocytes overexpressing ST18 showed upregulation of Conclusions: Our findings identify VDAC as a novel factor in the pathogenesis of PV and thus as an innovative and attractive therapeutic target for the treatment of this disease.
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