Abstract
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.