부산대학교 도서관

Chronic wounds are a frequent complication in diabetic patients and contribute significantly to morbidity and mortality. In the hyperglycaemic state, advanced glycation end products (AGEs) form, affecting collagen cross-linking, cytokine, nitric oxide and growth factor production and molecular signalling pathways. AGE receptors are upregulated and as it activates NF-kappaB, a host of inflammatory cytokines are expressed, exacerbating the self-sustaining inflammatory response seen in diabetic wounds. Therapeutic strategies include inhibiting the formation of AGEs, either directly or by inhibiting the formation of intermediates, and blocking the AGE receptor. A more complete understanding of the biology of the diabetic wound healing process is imperative in the development of successful treatment of diabetic wounds. [ABSTRACT FROM AUTHOR]