In recent years, coronary artery disease has become the world’s leading cause of death, and thus the global medical community has paid close attention to coronary artery disease and conducted multifaceted research on its treatment. The first percutaneous transluminal coronary angioplasty (PTCA) was performed in 1977, with a success rate of over 90%, however, the rate of coronary restenosis (RS) within 6 months after PTCA was 30-50%. The application of coronary artery intracoronary stenting (CASI) in the 1980s significantly reduced the incidence of coronary restenosis, but the clinical restenosis rate was still 20-30%. In recent years, the use of drug-coated stents has greatly reduced the rate of coronary restenosis, but because of the high cost of drug stents and their long-term restenosis rate has not been determined, the prevention and treatment of post-interventional restenosis, which is as important as drug and surgical treatment, has become a hot topic in the treatment of coronary heart disease. Studies have confirmed that the mechanical stimulation of the intima after coronary intervention causes the retraction of vascular elasticity and the release of vasoactive substances, which triggers the expression of oncogenes and cell cycle regulator genes, the result of which can cause early thrombosis and acute inflammatory response, proliferation of vascular smooth muscle cells (SMC), migration, formation of extracellular matrix and vascular remodeling resulting in restenosis after coronary intervention. After PTCA, vascular injury and endothelial debridement expose the subcutaneous tissue, causing immediate adhesion of platelets and leukocytes, leading to wall thrombus formation, and thrombus mechanization can directly cause intimal thickening. The endothelial cell-derived diastolic factor (NOEDRF) secreted by endothelial cells (EC) is reduced and the release of platelet-derived growth factor (PDGF) is increased, which promotes VSMC migration and activation and endothelial hyperplasia. post-CASI is mostly caused by endothelial hyperplasia, thrombosis and inflammatory response. The proliferating intima is mainly composed of proliferating migrating vascular smooth muscle cells (VSMC) and extracellular matrix. Mechanical damage to the endothelium after stenting exposes the subendothelial matrix and collagen, resulting in adhesion and aggregation of large numbers of platelets to form an appendage thrombus. Mechanical stimulation, endothelial injury, and mural thrombus can stimulate the increase of macrophages in tissues and neutrophils in blood. A large number of cytokines and growth factors can release mononuclear macrophages and platelets, which act on VSMC and eventually lead to the deposition of extracellular matrix and uncontrolled VSMC proliferation, resulting in PCI.