LAUSR

Psoriasis is a common chronic disease with accelerated epidermal cell growth. Solute carrier family 2 member 1 (SLC2A1), also named GLUT1, transports glucose and its analogues into cells. With elevated membrane‐bound GLUT1, psoriatic keratinocytes uptake more glucose with increased glucose metabolism. Competition between glucose and its analogues can serve as a strategy to inhibit glycolysis as well as proliferation. In this study, we investigated the expression patterns of GLUT1 in keratinocytes in the human psoriasis vulgaris and imiquimod‐induced psoriasis model, and determined that the glucose metabolism inhibitor 2‐deoxy‐D‐glucose (2‐DG) can relieve the psoriatic lesions. We found membrane‐enriched GLUT1 in psoriasis keratinocytes, which suggested some potential for glucose metabolic target therapy based on the glycolytic microenvironment. Furthermore, 2‐DG was able to relieve the psoriatic lesions in an in vivo animal model which provides a new possible therapeutic strategy.