Chemokine Regulation of Angiogenesis During Wound Healing.

Angiogenesis plays a critical role in wound healing. A defect in the formation of a neovasculature induces ulcer formation. One of the challenges faced by the clinician when devising strategies to promote healing of chronic wounds is the initiation of angiogenesis and the formation of a stable vasculature to support tissue regeneration. Understanding the molecular factors regulating angiogenesis during wound healing will lead to better therapies for healing chronic wounds. Classically, chronic wounds are treated with debridement to remove inhibitory molecules to reestablish angiogenesis and normal wound healing. The addition of platelet-derived growth factor (PDGF, becaplermin) has shown some promise as an adjunctive therapy, but better therapies are still needed. Current treatment strategies include investigating the outcome of augmenting cytokines locally to reduce the inflammatory response and promote angiogenesis. The failure of wounds to form a new vasculature results in the inability of the wound to fully heal, and thus may develop into a chronic ulcer if left untreated. Inhibition of neovascularization commonly results from an overactive inflammatory response that includes an excessive chemokine response. Therefore, understanding how the chemokine response regulates neoangiogenesis will enhance our ability to develop new treatment strategies to improve neovascularization and wound healing. The ability to regulate the chemokine environment in chronic wounds may enhance the development of the neovasculature to reduce invasive treatments and enhance wound healing. Either inhibiting chemokines that promote a chronic inflammatory response or increasing the levels of proangiogenic chemokines may enhance angiogenesis in chronic wounds.