Inflammation and fibrosis coupling contribute to hair follicle miniaturization in androgenetic alopeciaInflammation and Fibrosis Linked to Hair Loss in Male Pattern Baldness

Androgenetic alopecia (AGA) is primarily explained by genetic susceptibility and androgen-dependent signaling in dermal papilla cells. This mini-review examines whether low-grade, regionally heterogeneous perifollicular inflammation interacts with extracellular matrix remodeling as a complementary component of AGA pathobiology, without implying an autoimmune mechanism. Human AGA scalp studies report upper-follicular and perifollicular CD4+ lymphocytes, mast cells, immune-enriched transcriptional states, connective tissue sheath abnormalities, and fibrosis in subsets of patients. Patient-derived cells, ex vivo follicles, animal models, and cross-disease studies provide additional support for transforming growth factor-β, interleukin-6, prostaglandin D2, Wnt antagonism, oxidative stress, mitochondrial dysfunction, and cellular senescence. These signals could recruit or retain immune cells and shift dermal sheath cells or perifollicular fibroblasts toward matrix-producing and contractile states. Collagen accumulation, altered matrix turnover, stiffness, vascular restriction, and impaired epithelial–mesenchymal crosstalk may then reduce regenerative plasticity and stabilize miniaturization. Human evidence is strongest for androgen-dependent follicular stress and regional inflammatory or fibrotic changes. Specific immune-to-fibroblast circuits, mechanotransduction pathways, and their temporal sequence are supported mainly by experimental models or cross-disease evidence. Spatially resolved inflammation–fibrosis endotypes may help explain variation in treatment response and guide biomarker-enriched trials, but would not by themselves imply an autoimmune pathogenesis.