The Role of Fibrosis in Androgenetic Alopecia: Mechanisms and Implications

Background: Androgenetic alopecia (AGA) is a common pattern hair loss in which perifollicular fibrosis drives hair-follicle miniaturization. Inflammatory–fibrotic crosstalk centered on TGF-β/Smad, with input from Wnt/β-catenin and Notch, disrupts epithelial–mesenchymal communication and impairs regeneration. Summary: We summarize evidence linking chronic inflammation to fibroblast/myofibroblast activation and excessive extracellular-matrix deposition around hair follicles, highlight dermoscopic features that may reflect fibrotic burden, and outline a continuum between AGA and fibrosing patterned alopecias. We review anti-fibrotic strategies directed at TGF-β, Wnt/β-catenin and Notch signaling, and how combining anti-androgenic, anti-inflammatory and anti-fibrotic approaches could address both hormonal and structural drivers. Key Messages: • Perifollicular fibrosis is integral to AGA progression and may underlie incomplete treatment responses. • Dermoscopic signs such as perifollicular hyperpigmentation and whitish perifollicular structures may correlate with histologic fibrosis and merit validation. • Pathway-directed anti-fibrotic agents targeting TGF-β and Wnt/Notch show anti-fibrotic activity in other organs but require AGA-specific testing.