This study focuses on how diminished blood flow (ischemia) and the resultant trauma when blood flow is restored (reperfusion) contributes to pressure ulcer formation. To better understand cutaneous ischemia-reperfusion (I/R) injury, the researchers used a transgenic mouse line that expresses a transcription factor (SOX2) in the skin to show that SOX2 in skin cells suppresses oxidative stress and elevates amphiregulin production. Amphiregulin is a growth factor that may induce either cell proliferation or differentiation. The tissue-protective effect of SOX2 induction in keratinocytes was shown to significantly suppress vascular damage and hypoxic areas in cutaneous I/R injury through amphiregulin production.
What is exciting about this article?
Ischemia-reperfusion (I/R) injury is a key player in the pathogenesis of pressure ulcer formation. In this study, the researchers found that epidermal cells potentially regulate cutaneous I/R injury through amphiregulin production, resulting in the suppression of oxidative stress. Recombinant amphiregulin can be a potential therapeutic agent for cutaneous I/R injury.
Research reported in this publication was supported by the Intramural Research Program of the NIHʼs National Institute of Arthritis and Musculoskeletal and Skin Diseases.