Abstract
Occlusive artery disease (CAD) is the leading cause of death worldwide. Bypass graft surgery remains the most prevalently performed treatment for occlusive arterial disease, and veins are the most frequently used conduits for surgical revascularization. However, the clinical efficacy of bypass graft surgery is highly affected by the long-term potency rates of vein grafts, and no optimal treatments are available for the prevention of vein graft restenosis (VGR) at present. Hence, there is an urgent need to improve our understanding of the molecular mechanisms involved in mediating VGR. The past decade has seen the rapid development of genomic technologies, such as genome sequencing and microarray technologies, which will provide novel insights into potential molecular mechanisms involved in the VGR program. Ironically, high throughput data associated with VGR are extremely scarce. The main goal of the current study was to explore potential crucial genes and pathways associated with VGR and to provide valid biological information for further investigation of VGR. A comprehensive bioinformatics analysis was performed using high throughput gene expression data. Differentially expressed genes (DEGs) were identified using the R and Bioconductor packages. After functional enrichment analysis of the DEGs, protein–protein interaction (PPI) network and sub-PPI network analyses were performed. Finally, nine potential hub genes and fourteen pathways were identified. These hub genes may interact with each other and regulate the VGR program by modulating the cell cycle pathway. Future studies focusing on revealing the specific cellular and molecular mechanisms of these key genes and pathways involved in regulating the VGR program may provide novel therapeutic targets for VGR inhibition.
Highlights
Occlusive artery disease is a major cause of morbidity and mortality worldwide (Bansilal, Castellano & Fuster, 2015)
Despite development of novel treatments in past decades, coronary artery bypass graft (CABG) surgery remains the standard of care for patients with left main coronary artery disease (CAD) and three-vessel CAD (Serruys et al, 2009)
Clarifying the cellular and molecular mechanisms involved in vein graft restenosis (VGR) and identifying potential novel therapeutic targets for the prevention of restenosis are significant goals
Summary
Occlusive artery disease is a major cause of morbidity and mortality worldwide (Bansilal, Castellano & Fuster, 2015). Despite development of novel treatments in past decades, coronary artery bypass graft (CABG) surgery remains the standard of care for patients with left main coronary artery disease (CAD) and three-vessel CAD (Serruys et al, 2009). Most patients with late-stage peripheral artery occlusive disease are treated with peripheral artery bypass graft surgery (Weintraub et al, 2012). Due to their advantages in availability and length, veins are the most commonly used conduits in coronary and peripheral artery vascular surgeries (Goldman et al, 2004). No unequivocally effective treatments are available for vein graft failure (Elmore et al, 2016). Clarifying the cellular and molecular mechanisms involved in VGR and identifying potential novel therapeutic targets for the prevention of restenosis are significant goals
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