Abstract

Wound repair requires the concerted action of numerous cells and factors. The inflammation, proliferation, and remodeling phases of wound healing occur in a highly coordinated cascade. Angiogenesis, the formation of new blood vessels, is one of the critical steps in the proliferative phase of wound repair (1–5). Like wound healing, angiogenesis requires cell migration, proliferation, and extracellular matrix synthesis and assembly. New vessels provide nutrients to support the repair cells, promote granulation tissue formation, and facilitate the clearance of debris. Granulation tissue is mainly composed of blood vessels that also supply the necessary oxygen to stimulate repair. Wound angiogenesis is a complex multipstep process that involves many mediators. Despite a detailed knowledge about many angiogenic factors present in the wound, little progress has been made in defining the source of these factors and the regulatory events involved in their production (1–9). Further complicating the understanding of wound angiogenesis and repair is the fact that the mechanisms and mediators involved in repair likely vary depending on the depth of the wound, type of wound (burn, trauma, etc.), and the location (muscle, skin, bone, etc.). The condition and age of the patient (diabetic, paraplegic, on steroid therapy, elderly vs infant, etc) can also determine the rate of repair and response to angiogenic factors. Furthermore, the sex of the patient and hormonal status (premenopausal, postmenopausal, etc.) may also influence the repair mechanisms and responses. Impaired wound healing particularly affects the elderly and many of the 14 million diabetics in the United States and reduced angiogenesis is often a causative agent for wound-healing problems in these patient populations.

Full Text
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