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.

Grant support


Research Areas:

Cancer Biology Developmental Biology Genetics and Genomics Molecular Biology and Biochemistry Skin Biology


Keratinocyte-Specific SOX2 Overexpression Suppressed Pressure Ulcer Formation after Cutaneous Ischemia-Reperfusion Injury via Enhancement of Amphiregulin Production.

Inoue Y, Uchiyama A, Amalia SN, Ishikawa M, Kosaka K, Sekiguchi A, Ogino S, Yokoyama Y, Torii R, Hosoi M, Akai R, Iwawaki T, Morasso MI, Motegi SI
J Invest Dermatol.
2024 Jan;
doi: 10.1016/j.jid.2023.06.202
PMID: 37516309

Research reported in this publication was supported by the Intramural Research Program of the NIHʼs National Institute of Arthritis and Musculoskeletal and Skin Diseases.