The Role of Fibrosis in Androgenetic Alopecia: Mechanisms and Implications
November 2025
in “
Skin Appendage Disorders
”
androgenetic alopecia fibrosis perifollicular fibrosis hair-follicle miniaturization TGF-β/Smad pathway Wnt/β-catenin pathway Notch pathway inflammatory-fibrotic crosstalk extracellular matrix deposition perifollicular hyperpigmentation fibroblast activation anti-fibrotic strategies anti-androgenic treatments anti-inflammatory treatments AGA hair loss hair thinning anti-fibrotic agents
TLDR Fibrosis contributes to hair loss in androgenetic alopecia, and targeting it may improve treatment.
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 review suggests that chronic inflammation leads to fibroblast activation and excessive extracellular matrix deposition around hair follicles. It also notes that dermoscopic features like perifollicular hyperpigmentation may indicate fibrotic burden. The document advocates for anti-fibrotic strategies targeting these pathways and suggests that combining these with anti-androgenic and anti-inflammatory treatments could improve outcomes in AGA by addressing both hormonal and structural factors. However, it calls for AGA-specific testing of these anti-fibrotic agents.
