Skin diseases articles from across Nature Portfolio

STAT3-activated SPRR1B+ keratinocytes play a role in priming wound healing in oral mucosa, potentially contributing to an accelerated wound healing response compared to the skin.

Cell-cell adhesion by desmosomes is weakened in the blistering skin disease pemphigus vulgaris. Here, authors found that the transcription factor Kruppel-like factor 5 is essential for the expression of the desmosomal gene desmoglein 3 and suggest a novel treatment approach.

Wound healing mechanisms differ depending on the sex, particularly in chronic wounds. Therefore, sex should be considered in the design of nanomedicine- and biomaterials-based wound healing therapies, both in preclinical and clinical testing.

HIF-1 can regulate the cytotoxic activity of skin-infiltrating T cells in cutaneous lupus erythematosus and is a potential therapeutic target.

Patients with atopic dermatitis have fundamentally different skin microbial populations compared with people with healthy skin. Bacteria associated with atopic dermatitis express genes for survival in dry conditions and for ammonia production, modulating the pH of this distinct environment and driving complex ecological interactions.