Pathogenic Role of Diabetes-Induced Overexpression of Kallistatin in Corneal Wound Healing Deficiency Through Inhibition of Canonical Wnt Signaling

• DOI: 10.2337/db21-0740
• Publication Date: 2022-01-19T16:21:30Z
• Authors: Wentao Liang; Li Huang; Xiang Ma; Lijie Dong; Rui Cheng; Marcus Dehdarani; Dimitrios Karamichos; Jian-xing Ma
• Keywords: LRP6; LRP5

It was reported previously that circulation levels of kallistatin, an endogenous Wnt signaling inhibitor, are increased in patients with diabetes. The current study conducted to determine the role kallistatin delayed wound healing diabetic corneas. Immunostaining and Western blot analysis showed were upregulated corneas from humans rodents In murine corneal models, canonical activated nondiabetic suppressed corneas, correlating healing. Transgenic expression activation cornea Local inhibition by LRP6-blocking antibody, or soluble VLDL receptor ectodomain (an inhibitor) contrast, ablation resulted overactivation Wnt/β-catenin accelerated Activation promoted human epithelial cell migration proliferation, which attenuated kallistatin. Our findings suggested diabetes-induced overexpression contributes inhibiting signaling. Thus, could be potential therapeutic targets for complications.