No Evidence that Impaired Notch Signaling Differentiates Hidradenitis Suppurativa From Other Inflammatory Skin Diseases.

No Evidence that Impaired Notch Signaling Differentiates Hidradenitis Suppurativa From Other Inflammatory Skin Diseases.
Br J Dermatol. 2019 Oct 08;:
Authors: Frew JW, Navrazhina K
Abstract
The molecular pathogenesis of Hidradenitis Suppurativa (HS) is purported to involve Notch dysregulation secondary to sequence variants in components of the gamma secretase complex (GSC)1 . However, Notch dysregulation has also been identified in keratinocytes of other inflammatory dermatoses including psoriasis2 and atopic dermatitis2 . Animal knockout models of components of the GSC with resultant Notch dysregulation result in the development of dermal cysts and histological features of follicular occlusion, suggesting that aberrant Notch signaling is linked to the unique clinical and histological manifestations of HS3 . However, these models also rapidly develop multiple squamous cell carcinomas3 which is not consistent with the typical progression of HS. The precise role of Notch dysregulation as the primary driver in the molecular pathogenesis of HS is unclear. Dysregulated Notch signaling may be secondary to inflammation or other unknown molecular mechanisms, rather than an actual driver of HS2.
PMID: 31594026 [PubMed - as supplied by publisher]

Source: The British Journal of Dermatology - October 7, 2019 Category: Dermatology Authors: Frew JW, Navrazhina K Tags: Br J Dermatol Source Type: research