• Nathan B Menke, John W Cain, Angela Reynolds, David M Chan, Rebecca A Segal, Tarynn M Witten, Danail G Bonchev, Robert F Diegelmann, Kevin R Ward, and Virginia Commonwealth University Reanimation, Engineering Shock Center, The Wound Healing Group.
• Department of Emergency Medicine, Virginia Commonwealth University, Richmond, Virginia 23284-2014, USA.
• Wound Repair Regen. 2010 Jan 1;18(1):105-13.

AbstractThe complex interactions that characterize acute wound healing have stymied the development of effective therapeutic modalities. The use of computational models holds the promise to improve our basic approach to understanding the process. By modifying an existing ordinary differential equation model of systemic inflammation to simulate local wound healing, we expect to improve the understanding of the underlying complexities of wound healing and thus allow for the development of novel, targeted therapeutic strategies. The modifications in this local acute wound healing model include: evolution from a systemic model to a local model, the incorporation of fibroblast activity, and the effects of tissue oxygenation. Using these modifications we are able to simulate impaired wound healing in hypoxic wounds with varying levels of contamination. Possible therapeutic targets, such as fibroblast death rate and rate of fibroblast recruitment, have been identified by computational analysis. This model is a step toward constructing an integrative systems biology model of human wound healing.

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