Geoffrey C. Gurtner

TL;DR: Topical VEGF is able to improve wound healing by locally up-regulating growth factors important for tissue repair and by systemically mobilizing bone marrow-derived cells, including a population that contributes to blood vessel formation, and recruiting these cells to the local wound environment where they are able to accelerate repair.

TL;DR: A novel model of wound healing in mice utilizing wound splinting that is accurate, reproducible, minimizes wound contraction, and allows wound healing to occur through the processes of granulation and reepithelialization is described.

TL;DR: In this article, the authors reveal the presence of at least two fibroblast lineages in murine dorsal skin and identify CD26/DPP4 as a surface marker that allows isolation of this lineage.

TL;DR: It is demonstrated for the first time that mechanical stress applied to a healing wound is sufficient to produce hypertrophic scars in mice, and it is concluded that mechanical loading early in the proliferative phase of wound healing produces hypertrophic scar formation by inhibiting cellular apoptosis through an Akt‐dependent mechanism.

TL;DR: In vitro, diabetic fibroblasts show selective impairments in discrete cellular processes critical for tissue repair including cellular migration, VEGF production, and the response to hypoxia, which support a role for fibroblast dysfunction in the impaired wound healing observed in human diabetics, and suggest a mechanism for the poor clinical outcomes that occur after ischemic injury in diabetic patients.