ObjectiveTo investigate the role and potential mechanisms of neuropilin-1 (NRP1) in the pathogenesis of vein graft failure.MethodsThe rat vascular smooth muscle cells (VSMCs) were transfected with NRP1-shRNA adenovirus and negative control adenovirus respectively. Cell counting kit-8, flow cytometry, Transwell and Western blot were used to investigate the effects of inhibition of NRP1 on VSMCs proliferation viability, apoptosis, migration capacity and its downstream signaling pathway protein expression.ResultsThe proliferation and migration of rat VSMCs could be inhibited after down-regulation of NRP1, and the increase of apoptosis was also observed. Moreover, inhibition of NRP1 significantly reduced Akt and NF-κB phosphorylation in rat VSMCs, but had little effect on activation of ERK1/2.ConclusionNRP1 may promote vein graft hyperplastic remodeling by regulating the proliferation and migration of VSMCs through PI3K/Akt and NF-κB pathways, but further animal study is required.
The saphenous vein graft (SVG) remains the most commonly used conduit in coronary artery bypass grafting (CABG), yet its limited long-term patency adversely affects patient outcomes. SVG failure is a multistage pathological process, characterized by early thrombosis, intermediate intimal hyperplasia, and late atherosclerotic degeneration. These changes are driven by endothelial dysfunction induced by ischemia-reperfusion and mechanical injury, smooth muscle cell phenotypic modulation, inflammatory activation, and conventional cardiovascular risk factors. Preventive strategies for SVG failure have increasingly focused on both surgical and pharmacological optimization. Surgical approaches include appropriate target vessel and anastomotic site selection, refinement of SVG harvesting techniques (notably the no-touch technique and endoscopic vein harvesting), optimization of graft configurations, and routine intraoperative graft flow assessment. Postoperative secondary prevention is essential, as antithrombotic and lipid-lowering therapies have been shown to reduce SVG occlusion. In addition, emerging therapies, including gene-based interventions, antiproliferative agents, novel graft preservation solutions, and external vein graft supports, show promise in improving SVG durability. Integrated multimodal strategies may further reduce SVG failure and improve long-term outcomes after CABG. This article provides a review of researches related to SVG failure, including the mechanisms of failure, intraoperative preventive measures, pharmacological prevention, and recent advances in treatment, aiming to offer insights for clinical diagnosis, treatment and future studies.