Dapagliflozin Inhibits Thrombin Induced ADAM17 Phosphorylation and Downstream ERK/p-c-Jun-mediated CTGF Induction to Prevent Neointimal Hyperplasia

Key Points

• The research aims to explore the role of dapagliflozin in inhibiting thrombin-induced signaling that leads to vascular cell migration.
• In vitro analysis of VSMC (vascular smooth muscle cells) migration and signaling pathways
• Assessment of ADAM17 activation in response to thrombin
• Evaluation of ERK1/2 and c-Jun signaling.
• Examination of CTGF induction in the presence of dapagliflozin.
• Dapagliflozin significantly reduced thrombin-induced ADAM17 activation.
• Inhibition of ERK1/2-c-Jun signaling was observed with dapagliflozin treatment.
• CTGF induction linked to vascular injury was decreased, leading to reduced VSMC migration.