KLF4 modulates macrophage-driven inflammation in diabetic psoriasis-like dermatitis through the TIMP3-ADAM17 axis: A basic research.

This study investigated the role of Krüppel-like factor 4 (KLF4) in macrophage-mediated inflammation in type 2 diabetes mellitus (T2DM) with psoriasis. KLF4, tissue inhibitor of metalloproteinases 3 (TIMP3), and a disintegrin and a metalloproteinase domain 17 (ADAM17) levels were measured in skin samples from patients. A diabetic psoriasis-like dermatitis mouse model was established using imiquimod (IMQ) and treated with KLF4-overexpressing lentiviruses. Glucose/lipid metabolism, skin pathology, mast cell counts, and inflammatory markers were assessed. Macrophage status was evaluated by F4/80 staining. KLF4 was downregulated in patients with T2DM with psoriasis. In mice with diabetic psoriasis-like dermatitis. KLF4 overexpression improved glucose/lipid metabolism and reduced skin erythema, scaling, thickening, psoriasis area severity index scores, and mast cell infiltration. KLF4 also decreased inflammation and modulated the TIMP3/ADAM17 pathway. These findings indicate that KLF4 ameliorates IMQ-induced inflammation via the TIMP3/ADAM17 pathway in diabetic psoriasis-like dermatitis.