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This study found a significant overlap between gene expression signatures of alopecia areata and certain chronic inflammatory skin disorders, suggesting shared biological processes may drive their co-occurrence and providing a foundation for future research into distinct comorbid subtypes.

This review highlights that disturbances in neuroimmune communication, particularly between sympathetic nerves and macrophages, may contribute to autoimmune diseases like rheumatoid arthritis and type 1 diabetes, and suggests potential therapeutic avenues by restoring this communication in preclinical and early clinical studies.

In this study, researchers identified that keloid fibroblasts respond to neurotransmitters from catecholaminergic nerves by producing bone matrix proteins, mediated by β1-adrenergic receptor activation, leading to fibro-osseous reprogramming; blocking this signaling in a rodent model prevented the development of keloid-like pathology.

This narrative review explores how psychological stress may contribute to premature skin aging by affecting dermal collagen and elastin remodeling through neuroendocrine, molecular, and cellular pathways, highlighting potential therapeutic targets to preserve skin structure and function.

This study found that in androgenetic alopecia, reduced stem cell factor production by dermal papilla cells may lead to decreased pigmentation in hair follicles.