Tenascin-C: a key molecule in graft stenosis.

摘要

Coronary artery bypass grafting (CABG) using venous and arterial grafts is a standard surgical procedure for the treatment of advanced coronary artery disease. However graft failure is common especially after transplantation of saphenous vein grafts, the first vessels used in CABG , After one year up to 15% and after 10 years up to 50% of saphenous vein grafts are severely affected by neointimal thickening and advanced atherosclerosis. Improved long-term patency and survival in treatment of advanced coronary artery disease has been achieved by the use of arterial grafts from the left internal thoracic (mammary) artery and other arteries such as the right internal thoracic artery or the radial artery . However, atherosclerosis and neointimal thickening especially at the site of anastomosis reduce the clinical success of by-pass grafting still today. Therefore, the search for novel therapeutic targets for prevention of graft failure continues. The paper by Sawada et al. in the current issue of Cardiovascular Research addresses the role and origin of tenascin-C (TN-C) during neointimal hyper-plasia in a mouse model of aorta-to-carotid artery interposition grafting.