<正>Percutaneous transluminal angioplasty has become a mainstay in the treatment of both carotid and coronary ischemic diseases due to hypertension and diabetes-induced atherosclerosis. The effectiveness of this therapy is severely compromised by its major complication restenosis, which is characterized by neointimal formation and intimal hyperplasia. Restenosis occurs in 10-30% of patients despite the currently employed stenting therapies. Endothelial nitric oxide (NO) protects blood vessels by inhibiting platelet and leukocyte adhesion, suppressing smooth muscle proliferation and migration, and promoting endothelial survival and proliferation. At sites of vascular injury following angioplasty, the endothelium is disrupted and NO synthesis is impaired.
GTP cyclohydrolase and restenosis;eNOS;
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