Physiology and pathophysiology of wound healing in diabetes

Abstract

Wound healing is an evolutionary conserved process that aims to restore the damaged barrier. This complex process involves many cellular responses including inflammation, proliferation, migration, angiogenesis, and tissue remodeling. Immediately after the injury, blood components are released into the wound site, activating the clotting cascade. The resulting clot induces hemostasis and provides a matrix for the influx of inflammatory cells. Inflammation is characterized by leukocyte migration and arrival to the site of injury. Neutrophils arrive first to remove contaminating bacteria (Singer and Clark, N Engl J Med 341(10):738-746, 1999) and are followed by monocytes, which differentiate into macrophages. Macrophages play an important role in augmenting the inflammatory response and tissue debridement. At the same time, many different cell types respond to initial inflammatory signals and start migrating to the wound site, including keratinocytes, endothelial cells, and circulating and local progenitor cells.