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March 5, 2026Cardiovascular Drugs and Therapy0 citationsOpen Access

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

TYTing-Lin YenPCPo-Ching ChouCTChia-Ti Tsai Tsai

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.

Abstract

Dapagliflozin inhibits thrombin-induced ADAM17 activation and downstream ERK1/2-c-Jun-CTGF signaling, thereby limiting VSMC migration and neointimal formation after vascular injury. This SGLT2-independent mechanism provides new insight into the pleiotropic vasculoprotective actions of dapagliflozin and identifies ADAM17 as a potential therapeutic target for preventing vascular restenosis and fibrosis-related cardiovascular disease.

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Cite This Study

Yen et al. (2026) studied this question.

synapsesocial.com/papers/69a91da8d6127c7a504c0b38https://doi.org/10.1007/s10557-026-07857-8
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