Dapagliflozin Inhibits Thrombin Induced ADAM17 Phosphorylation and Downstream ERK/p-c-Jun-mediated CTGF Induction to Prevent Neointimal Hyperplasia
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.
Authors
- Chieh‐Yu Chen (ORCID: https://orcid.org/0000-0001-8315-0781)
- Ting-Lin Yen
- Chia-Ti Tsai Tsai
- Wen-Chin Ko
- Po-Ching Chou
- Yi-Ling Chen
- Yi-Fan Chien
Institutions
- Fu Jen Catholic University (TW)
- Cathay General Hospital (TW)
- National Taiwan University Hospital (TW)
- Taipei Medical University (TW)
Publication Details
- Journal
- Cardiovascular Drugs and Therapy
- Published
- 2026-03-03
- DOI
- https://doi.org/10.1007/s10557-026-07857-8
- Primary Topic
- Connective Tissue Growth Factor Research
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Cathay General Hospital