Supplementary Material for: The Role of Fibrosis in Androgenetic Alopecia: Mechanisms and Implications
January 2025
androgenetic alopecia perifollicular fibrosis hair-follicle miniaturization TGF-β/Smad pathway Wnt/β-catenin pathway Notch pathway chronic inflammation dermoscopic features perifollicular hyperpigmentation anti-fibrotic strategies anti-androgenic treatments anti-inflammatory treatments anti-fibrotic treatments AGA fibrosis hair loss inflammation hair regeneration
TLDR Combining anti-androgenic, anti-inflammatory, and anti-fibrotic treatments may improve hair loss outcomes.
This document discusses the role of fibrosis in androgenetic alopecia (AGA), highlighting how perifollicular fibrosis contributes to hair-follicle miniaturization and hair loss. It emphasizes the involvement of inflammatory-fibrotic crosstalk, particularly through TGF-β/Smad, Wnt/β-catenin, and Notch pathways, which disrupts communication necessary for hair regeneration. The document reviews evidence linking chronic inflammation to fibrosis around hair follicles and suggests that dermoscopic features like perifollicular hyperpigmentation may indicate fibrotic burden. It also explores anti-fibrotic strategies targeting these pathways and suggests that combining anti-androgenic, anti-inflammatory, and anti-fibrotic treatments could improve outcomes by addressing both hormonal and structural factors. However, the efficacy of these anti-fibrotic agents in AGA requires further testing.
