Keratinocyte Growth Factors in Wound Healing

Keratinocyte growth factors (KGFs), primarily fibroblast growth factor-7 (FGF-7) and related family members, are secreted by mesenchymal cells and act as potent epithelial mitogens. Binding to the FGFR2b receptor on keratinocytes, these factors activate intracellular signalling pathways—such as MAPK, PI3K/AKT and STAT—that orchestrate keratinocyte proliferation, migration and differentiation. Through paracrine interactions with fibroblasts and immune cells, KGFs also contribute to extracellular matrix remodelling, angiogenesis and modulation of local inflammation. In acute wounds, timely KGF signalling promotes efficient re-epithelialisation, whereas in chronic or diabetic ulcers, dysregulated KGF expression can impede barrier restoration. Recombinant KGFs and engineered analogues have shown promise in accelerating wound closure, reducing scar formation and enhancing epidermal barrier function, highlighting their global significance in regenerative therapies.

Research from Nature Portfolio

Studies using conditional gene knockout in murine models have revealed that targeted ablation of neural-Wiskott Aldrich syndrome protein (N-WASP) in fibroblasts leads to elevated expression of FGF-7, accelerated keratinocyte proliferation and enhanced collagen deposition. The absence of N-WASP in fibroblasts improved contraction and re-epithelialisation in excisional wound models, demonstrating that modulation of stromal actin dynamics can potentiate keratinocyte growth factor–driven repair.

Keratinocyte Growth Factors in Wound Healing publication trend

The graph below shows the total number of articles in keratinocyte growth factors in wound healing across all publications each year (not limited to Nature Index journals).

Technical terms

Keratinocyte Growth Factor (KGF): A paracrine member of the fibroblast growth factor family (FGF-7) that stimulates epithelial cell proliferation and migration.

FGFR2b: A splice variant of the fibroblast growth factor receptor 2, expressed on epithelial cells, that mediates responses to KGFs.

Paracrine signalling: The process by which cells secrete factors that act on neighbouring cells to regulate their behaviour.

Re-epithelialisation: The restoration of an intact epithelial layer over a wound surface through keratinocyte migration and proliferation.

References

1. Bioengineered MSCCxcr2 transdifferentiated keratinocyte-like cell-derived organoid potentiates skin regeneration through ERK1/2 and STAT3 signaling in diabetic wound. Cellular and Molecular Life Sciences (2024).
2. KGF-1 accelerates wound contraction through the TGF-β1/Smad signaling pathway in a double-paracrine manner. Journal of Biological Chemistry (2019).
3. Fibroblast Growth Factor in Diabetic Foot Ulcer: Progress and Therapeutic Prospects. Frontiers in Endocrinology (2021).
4. Conditional knockout of N-WASP in mouse fibroblast caused keratinocyte hyper proliferation and enhanced wound closure. Scientific Reports (2016).