Our ability to heal wounds deteriorates with age, leading in many cases to a complete lack of repair and development of a chronic wound. Moreover, as the elderly population continues to grow the prevalence of non-healing chronic wounds is escalating. Cutaneous wound repair occurs through a combination of overlapping phases, including an initial inflammatory response, a proliferative phase and a final remodelling phase. In elderly subjects the inflammatory response is delayed, macrophage and fibroblast function compromised, angiogenesis reduced and re-epithelialization inhibited. Whilst a large body of historic research describes the defective processes that lead to delayed healing, only recently have the molecular mechanisms by which these defects arise begun to be elucidated. Current therapies available for treatment of chronic wounds in elderly people are surprisingly limited and generally ineffective. Thus there is an urgent need to develop new therapeutic strategies based on these recent molecular and cellular insights.

Wound healing is a complex process that we have only recently begun to understand. Central to wound repair is transforming growth factor β (TGF-β), a cytokine secreted by several different cell types involved in healing. TGF-β has diverse effects, depending upon the tissue studied. This review focuses on healing in skin, particularly the phases of cutaneous wound repair and the role of TGF-β in normal and impaired wound-healing models. It also explores TGF-β activity in scarless foetal wound healing. Knowledge of TGF-β function in scarless repair is critical to improving healing in clinical scenarios, such as diabetic wounds and hypertrophic scars.