Acute and chronic wounds are a source of significant morbidity for patients, and they demand a growing portion of health-care time and finances to be devoted to their care. Transforming growth factor-β (TGF-β) has surfaced from abundant research as a key signal in orchestrating wound repair. In beginning this review, we discuss the inflammatory, proliferative, and maturational phases of wound healing. We then focus on TGF-β by first discussing the pathway from its production to the target cell where Smad proteins execute an intracellular signaling cascade. To review TGF-β's role in wound healing, we discuss the actions of it individually on keratinocytes, fibroblasts, endothelial cells, and monocytes, which are the major cell types involved in wound repair. From illustrating these cellular actions of TGF-β, we summarize its multipotent role in the process of wound repair. As a clinical correlation, we also review research dedicated to the involvement of TGF-β in venous stasis ulcers.

In a patient with multiple trauma, blunt thoracic trauma with concomitant aortic disruption is often eminently lethal, ranking second to head injury as the most common cause of trauma-related deaths. Open surgical repair of the aortic lesion has morbidity and mortality rates that are among the highest in the field of cardiovascular surgery. Results with thoracic endovascular aortic repair for traumatic aortic disruption are promising. The facility requirements, technique, and early results of thoracic endovascular aortic repair for the treatment of this difficult aortic injury are presented.

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