Abstract:

BACKGROUND: Great saphenous vein is the most common vascular material in coronary artery bypass grafting, however, the graft neointimal hyperplasia and subsequent atherosclerosis result in angiostegnosis, which affect the long-term efficacy.
OBJECTIVE: To analyze the pathophysiology and mechanism of the angiostenosis, additionally, to construct smooth muscle cell specific SM22α promoter and SMHC enhancer.
METHODS: The database of PubMed, HighWire and CNKI were retrieved with key words of “SM22α promoter, SMHC enhancer, stenosis, Pi3k and RNAi/RNA interference”. The language was confined to English and Chinese. The literatures correlated with angiostenosis, VSMC-specific SM22α promoter and enhancer were selected. The reviews and overlapped researches were excluded. In vascular smooth muscle cell proliferation and apoptosis of graft neointimal hyperplasia, as well as the extent of graft thrombosis were considered as evaluation index.
RESULTS AND CONCLUSION: More than 8 730 literatures were searched by the computer. According to inclusion and exclusion criteria, the SM22α promoter and angiostenosis were analyzed. The neointimal hyperplasia and thrombosis had a strong impact on prospective efficacy after coronary artery bypass grafting. The PI3K-Akt-mTOR pathway was a crucial signal passage which regulated cell proliferation and migration. RNA interference targeting Pik3cb can efficiently suppress the neointimal hyperplasia through down regulating the PI3K-Akt-mTOR pathway. The shRNA eukaryon expression plasmid vectors targeting rat Pik3cb were constructed using VSMC-specific SM22α promoter. On the one hand, it can suppress the neointimal hyperplasia, and on the other, it can prevent the occurrence of thrombosis.SM22α is a specific gene in vascular smooth muscle cell. The studies that applied VSMC-specific SM22α promoter/enhancer to vascular grafting provide a new strategy to prevent angiostenosis and thrombosis.