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This study found that skin organoids derived from iPSCs with an HS-associated NCSTN mutation showed defects in hair follicle stem cell differentiation and increased expression of inflammatory proteins related to hidradenitis suppurativa.

This study suggests that the NCSTN knockout mouse could serve as an HS animal model, with tamoxifen potentially used for gene deletion in mice.

This article offers a viewpoint on hidradenitis suppurativa pathogenesis, suggesting that impaired Notch signalling from γ-secretase mutations may drive inflammation and link the condition to other Th17-driven diseases.

This review discusses the genetic, autoinflammatory, and keratinization factors involved in hidradenitis suppurativa and presents the concept of classifying it as an autoinflammatory keratinization disease, but reports no new clinical results.

This study found that the PSEN1-P242LfsX11 mutation in hidradenitis suppurativa influences cytokine and chemokine expression in macrophages, potentially affecting inflammatory responses.