Mechanisms of normal versus diabetic wound healing. In a normal wound, macrophages combat wound bed pathogens, while fibroblasts deliver VEGF to initiate regrowth of epithelial cells and close the open wound. In diabetic wounds, insufficient angiogenesis and macrophage function result in significant pathogen invasion, while lower fibroblast presence delays re‐epithelization and wound closure.

Diabetic Wound Healing

Chronic wounds, such as pressure ulcers, vascular ulcers, and diabetic ulcers, affect between 2.4 and 4.5 million people in the United States, causing a significant humanistic and financial burden. Such chronicity can have severe ramifications for diabetic patients, as chronic wounds are the leading cause of diabetes‐associated amputations. Due to the threat of chronic wounds to diabetic health and the increasing prevalence of diabetes, many researchers have focused on developing more effective strategies for wound treatment.

Nitric oxide, NO, represents a potential wound therapeutic agent due to its ability to regulate inflammation and eradicate bacterial infections. Two broad strategies exist to utilize NO for wound healing; liberating NO from endogenous reservoirs, and supplementing NO from exogenous sources.

In a progress report, published in Advanced Healthcare Materials, graduate students Maggie J. Malone‐Povolny and Sara E. Maloney in the the Schoenfisch Group, examine the efficacy of a variety of NO‐based methods to improve wound outcomes, with particular attention given to diabetes‐associated chronic wounds.