Colchicine Prevents Intimal Hyperplasia in Venous Bypass Grafts

All articles of this category (opens in new window) Background: Intimal hyperplasia is the leading cause of venous graft failure. Initial endothelial cell (EC) damage triggers the recruitment of leukocytes, which, through inflammation, induce migration and proliferation of vascular smooth muscle cells (VSMCs) within the venous wall. These processes are similar to those in atherosclerosis. Recent clinical studies have highlighted colchicine as an effective secondary prophylaxis for preventing atherosclerosis progression. This study aims to investigate the effects of colchicine on intimal hyperplasia, leveraging its anti-inflammatory and anti-proliferative properties to prevent venous graft failure. Methods: Cell culture experiments were conducted using human endothelial cells and human vascular smooth muscle cells. Dose-response assays were performed to determine the effects of colchicine on proliferation and apoptosis in both cell types. ECs were treated with an inflammatory stimulus, and Vascular Cell Adhesion Molecule 1 (VCAM-1) expression was measured using qPCR. Monocyte adhesion was analyzed by co-culturing ECs with fluorescence-labeled monocytes. VSMC migration and proliferation were assessed using scratch and transwell migration assays. An in vivo venous bypass model was established in C57Bl/6J mice by interposing a donor inferior vena cava (IVC) into the carotid artery. Mice in the treatment group received colchicine in drinking water for 4 weeks. Subsequently, intimal hyperplasia of the venous grafts was evaluated histologically. Results: Colchicine inhibited the proliferation of both VSMCs and ECs in a dose-dependent manner, as expected. Notably, even at high concentrations, colchicine did not induce excessive apoptosis. Moreover, colchicine effectively prevented leukocyte adhesion to ECs following inflammatory stimulation by inhibiting the upregulation of VCAM-1. Colchicine significantly reduced VSMC proliferation and migration, as demonstrated by the scratch assay. Transwell migration assays confirmed a decrease in VSMC motility in vitro following colchicine treatment. In vivo, colchicine treatment reduced intimal hyperplasia of venous grafts and was associated with a decreased αSMA-positive area compared with controls. Conclusion: Colchicine effectively inhibits key processes involved in intimal hyperplasia by reducing endothelial activation, leukocyte adhesion, and vascular smooth muscle cell proliferation and migration. These findings support the use of colchicine as a promising approach to improve venous graft patency and prevent graft failure in bypass surgery. Publication History Article published online: 17 February 2026 © 2026. Thieme. All rights reserved. Georg Thieme Verlag KG Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany