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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:1679.)
© 2007 American Heart Association, Inc.

Editorials

Emerging Role of IGF-1R in Stretch-Induced Neointimal Hyperplasia in Venous Grafts

Hannah Song; Amy L. Mowbray; Michelle C. Sykes; Hanjoong Jo

From the Wallace H. Coulter Department of Biomedical Engineering (H.S., M.C.S., A.L.M., H.J.), Georgia Institute of Technology and Emory University, and Division of Cardiology (H.J.), Emory University, Atlanta, Ga.

Correspondence to Hanjoong Jo, PhD, Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University, 2005 WMB, Atlanta, GA 30322. E-mail hanjoong.jo@bme.gatech.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Autologous saphenous veins are commonly used to circumvent occluded coronary arteries during coronary artery bypass grafting (CABG) procedures.¹ Although these vessels provide an effective treatment for myocardial ischemic disease, they are susceptible to accelerated atherosclerosis and fail in 50% of cases within 10 years of surgery.^2–4 Venous graft disease occurs via 3 temporally distinct processes including thrombosis, neointimal hyperplasia, and atherosclerosis with each process contributing significantly to the onset of the next. During neointimal hyperplasia, vascular smooth muscle cells (VSMCs) and extracellular matrix accumulate in the intimal region causing intimal thickening and narrowing of the vessel lumen.^3–5 Even though the disease process has been described, the detailed mechanisms behind the cellular events are unclear. In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Cheng and Du illustrate a novel underlying mechanism involving an insulin-like growth factor (IGF-1) and IGF-1 receptor (IGF-1R) pathway by which cyclic stretch of VSMC plays a critical role in intimal thickening of venous grafts.

See page 1744

Blood flow generates a wide range of hemodynamic forces including frictional wall shear stress, circumferential stress, and compressive stress.⁶ Arteries are exposed to cyclic circumferential stretch attributable to pulsatile blood flow. Furthermore, they experience higher pressures than veins. Whereas the endothelium is constantly subjected to fluid shear stress, the underlying layers of smooth muscle cells are exposed mainly to circumferential stretch. It has been well established that altered mechanical forces cause dysregulated cellular phenotypes and contribute to pathology in disease conditions such as hypertension, atherosclerosis, and venous graft . . . [Full Text of this Article]

Related Article:

Mechanical Stretch Simulates Proliferation of Venous Smooth Muscle Cells Through Activation of the Insulin-Like Growth Factor-1 Receptor

Jizhong Cheng and Jie Du
Arterioscler Thromb Vasc Biol 2007 27: 1744-1751. [Abstract] [Full Text] [PDF]