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Hair follicle fibrosis

Molecular classification
Other (as a process; not a receptor, enzyme, transporter, etc.)
01

Overview

Hair follicle fibrosis refers to the pathological accumulation of extracellular matrix and connective tissue (mainly collagen) around or within hair follicles, usually leading to permanent damage of the follicle architecture and irreversible hair loss. Fibrosis can result from chronic inflammation, autoimmune reactions, or persistent injury, and is characterized by the activation of fibroblasts and upregulation of fibrogenic pathways such as transforming growth factor-beta (TGF-β). This process is prominent in primary cicatricial (scarring) alopecias and other fibrosing skin diseases. While various signaling pathways (TGF-β/SMAD, Wnt, BMP, etc.) are implicated in the regulation of hair follicle cells and their response to injury and fibrosis[2][3], "hair follicle fibrosis" by itself is not a molecular target but a disease mechanism. Drugs that reduce hair follicle fibrosis typically act by modulating inflammatory and fibrogenic signaling rather than interacting with a single receptor or protein.

Other names
Follicular fibrosisPerifollicular fibrosis
02

Mechanism of action

Inhibition of inflammatory cytokines, inhibition of fibroblast activation, reduction of extracellular matrix deposition; for molecular targets, typical mechanisms include TGF-β inhibition, immune modulation

03

Biological functions

FibrosisExtracellular matrix remodelingWound healing response
04

Disease associations

Hair loss disorders (such as lichen planopilaris, cicatricial alopecia)Other fibrotic skin conditions
05

Safety considerations

Potential adverse effects of immunosuppressive or anti-fibrotic therapiesrisk of skin atrophy with topical steroids
06

Interacting drugs

Drugs targeting fibrotic pathways or inflammation (e.g., corticosteroids, immunosuppressants, anti-fibrotic agents such as pirfenidone)
07

Biomarkers

Increased collagen deposition in hair follicle sheathupregulation of fibrotic markers (e.g., TGF-β, alpha-SMA, collagen I/III)loss of hair follicle stem cell markers

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