Expression of AKR1C3 Protein in Human Keloid Skin Tissue

Abstract

Keloids are among the most noticeable types of scars and may occur as a result of abnormal wound healing. They are formed by deposition of extracellular matrix components and proliferation of fibroblasts [1]. Keloids compose a pathologic condition characterized by the presence of hyalinized collagen bundles and the existence of chronic inflammatory reactions, such as oxidative stress [2]. Keloid scars extend beyond the margin of the original wound compared with hypertrophic scars. Keloids are estimated to occur in about 10% of people [3] and are seen more often in people with highly pigmented skin such as Black and Asian people rather than Caucasian people [4]. The pathophysiological basis of keloids is yet to be completely determined. There have been many ongoing keloid-related studies because keloids cause serious functional and aesthetic problems. However, there are no uniformly successful treatments for keloid scars. Excision and primary repair frequently result in recurrence. It was recently reported that keloid formation is associated with reactive oxygen species (ROS) [3]. According to De Felice et al. [3], significant increases in ROS in keloid tissue fibroblasts are related to oxidative injury and inflammatory reaction. ROS, including superoxide anion (O), hydrogen peroxide (H2O2), and hydroxyl anion (OH), can oxidize and modify intracellular molecules. ROS production is induced either directly by oxidants/ oxidases or by a decrease in antioxidants and related upregulation of oxidative damage-inducible genes [2,5]. ROS can directly destroy both DNA and proteins. ROS play a crucial role in the apoptosis of cells injured by oxidation, especially in inflammatory cells Doo Hyun Nam, DaWoon Lee, Chul Han Kim, Sang Gue Kang, Ho Seong Shin, Young Man Lee