# Fibroblast Growth Factor-7 and Hair Biology: Bridging Basic Science and Therapeutic Applications

**Authors:** Huey-Chun Huang, Wang-Ju Hsieh, Ivona Percec, Tsong-Min Chang

PMC · DOI: 10.3390/cimb48010102 · Current Issues in Molecular Biology · 2026-01-19

## TL;DR

Fibroblast Growth Factor-7 (FGF-7) promotes hair growth by activating key signaling pathways and could lead to new hair regeneration therapies.

## Contribution

The paper highlights FGF-7's role in hair biology and its potential as a novel therapeutic target for hair regeneration.

## Key findings

- FGF-7 activates FGFR2b to promote keratinocyte proliferation and hair follicle growth.
- FGF-7 synergizes with IGF-1 and VEGF to enhance follicular regeneration.
- Topical FGF-7 is safe, but systemic use requires monitoring due to potential side effects.

## Abstract

Alopecia profoundly impacts psychological well-being and quality of life, yet current therapeutic options such as minoxidil and finasteride exhibit limited efficacy. Fibroblast growth factor 7 (FGF-7), also known as keratinocyte growth factor (KGF), is a paracrine growth factor secreted by dermal papilla cells that specifically activates the epithelial receptor FGFR2b. Receptor engagement triggers multiple downstream signaling cascades, including the MAPK/ERK, PI3K/Akt, and Wnt/β-catenin pathways, promoting keratinocyte proliferation, stem cell activation, and the transition of hair follicles into the anagen phase. Both in vitro and in vivo animal studies consistently demonstrate that FGF-7 accelerates telogen-to-anagen transition and enhances follicular regeneration. FGF-7 acts synergistically with insulin-like growth factor 1 (IGF-1) and vascular endothelial growth factor (VEGF) to sustain nutrient delivery and cell proliferation. Human scalp studies further reveal a strong association between the FGF-7/FGFR2b signaling and follicular activity; however, clinical trials remain scarce. Topical application of FGF-7 has demonstrated an excellent safety profile, whereas systemic administration necessitates careful monitoring. Future directions include the development of engineering to extend the systemic half-life, advanced delivery systems, and gene or mRNA-based therapeutic approaches. Thus, the FGF-7/FGFR2b axis is a highly compelling molecular target for next-generation hair regeneration therapies.

## Linked entities

- **Genes:** FGF7 (fibroblast growth factor 7) [NCBI Gene 2252], Fgfr2 (fibroblast growth factor receptor 2) [NCBI Gene 14183]
- **Proteins:** FGF7 (fibroblast growth factor 7), IGF1 (insulin like growth factor 1), VEGFA (vascular endothelial growth factor A), Fgfr2 (fibroblast growth factor receptor 2)
- **Diseases:** Alopecia (MONDO:0004907)

## Full-text entities

- **Genes:** AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, FGFR2 (fibroblast growth factor receptor 2) [NCBI Gene 2263] {aka BBDS, BEK, BFR-1, CD332, CEK3, CFD1}, CTNNB1 (catenin beta 1) [NCBI Gene 1499] {aka CTNNB, EVR7, MRD19, NEDSDV, armadillo}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, MAPK1 (mitogen-activated protein kinase 1) [NCBI Gene 5594] {aka ERK, ERK-2, ERK2, ERT1, MAPK2, NS13}, IGF1 (insulin like growth factor 1) [NCBI Gene 3479] {aka IGF, IGF-I, IGFI, MGF}, FGF7 (fibroblast growth factor 7) [NCBI Gene 2252] {aka HBGF-7, KGF}
- **Diseases:** Alopecia (MESH:D000505)
- **Chemicals:** minoxidil (MESH:D008914), finasteride (MESH:D018120)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12839674/full.md

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12839674/full.md

## References

102 references — full list in the complete paper: https://tomesphere.com/paper/PMC12839674/full.md

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Source: https://tomesphere.com/paper/PMC12839674