Abstract
Effective healing of skin wounds is essential for our survival. Although skin has strong regenerative potential, dysfunctional and disfiguring scars can result from aberrant wound repair. Skin scarring involves excessive deposition and misalignment of ECM (extracellular matrix), increased cellularity, and chronic inflammation. Transforming growth factor-β (TGFβ) signaling exerts pleiotropic effects on wound healing by regulating cell proliferation, migration, ECM production, and the immune response. Although blocking TGFβ signaling can reduce tissue fibrosis and scarring, systemic inhibition of TGFβ can lead to significant side effects and inhibit wound re-epithelization. In this study, we develop a wound dressing material based on an integrated photo-crosslinking strategy and a microcapsule platform with pulsatile release of TGF-β inhibitor to achieve spatiotemporal specificity for skin wounds. The material enhances skin wound closure while effectively suppressing scar formation in murine skin wounds and large animal preclinical models. Our study presents a strategy for scarless wound repair.
Highlights
Effective healing of skin wounds is essential for our survival
It has been shown that three isoforms (1-3) of Transforming growth factor-β (TGFβ) may have different temporal effects on skin wound repair and scar formation, and disruption of their expression may lead to hypertrophic scarring[14,15,17,18,19,20,21,22,23]
Our results further show that pulsatile release of the TGF-β inhibitor can accelerate skin wound closure while suppressing scarring in murine skin wounds and large animal preclinical models, suggesting that it could be an effective approach to achieve scarless wound healing in skin
Summary
Effective healing of skin wounds is essential for our survival. skin has strong regenerative potential, dysfunctional and disfiguring scars can result from aberrant wound repair. Wound repair in skin involves four different stages: hemostasis, inflammation, re-epithelization, and resolution/tissue remodeling[1,2,3]. TGFβ has been well-recognized as a key regulator of skin wound repair[7,14,15,16] It exerts pleiotropic effects on different phases of wound healing by regulating proliferation of epidermal and dermal cells, epithelial cell migration, ECM production, and the immune response. Our results further show that pulsatile release of the TGF-β inhibitor can accelerate skin wound closure while suppressing scarring in murine skin wounds and large animal preclinical models, suggesting that it could be an effective approach to achieve scarless wound healing in skin
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