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Updated: Nov 28, 2025
A Rabbit Model of Durable Transgene Expression in Jugular Vein to Common Carotid Artery Interposition Grafts
Published on: September 10, 2018
BPI and KIR6.1 as significant hub genes for vein graft restenosis
Yun-Peng Bai1, Bo-Chen Yao1, Mei Wang2
1Department of Cardiac Surgery, Tianjin Chest Hospital, Tianjin, P. R. China.
Background:
Vein graft restenosis (VGR), which appears to be caused by dyslipidemia following vascular transplantation, seriously affects the prognosis and long-term quality of life of patients.
Methods:
This study analyzed the genetic data of restenosis (VGR group) and non-stenosis (control group) vessels from patients with coronary heart disease post-vascular transplantation and identified hub genes that might be responsible for its occurrence. GSE110398 was downloaded from the Gene Expression Omnibus database. A repeatability test for the GSE110398 dataset was performed using R language. This included the identification of differentially expressed genes (DEGs), enrichment analysis via Metascape software, pathway enrichment analysis, and construction of a protein-protein interaction network and a hub gene network.
Results:
Twenty-four DEGs were identified between VGR and control groups. The four most important hub genes (KIR6.1, PCLP1, EDNRB, and BPI) were identified, and Pearson's correlation coefficient showed that KIR6.1 and BPI were significantly correlated with VGR. KIR6.1 could also sensitively predict VGR (0.9 < area under the curve ≤1).
Conclusion:
BPI and KIR6.1 were differentially expressed in vessels with and without stenosis after vascular transplantation, suggesting that these genes or their encoded proteins may be involved in the occurrence of VGR.
