Vascular bypass graft failure is a significant clinical problem and is frequently due to the formation of intimal hyperplasia (IH) [1–3]. IH is characterized by the accumulation of smooth muscle cells (SMC) and extracellular matrix in the intima of the vessel, which occurs when the normal balance between vascular cell proliferation and apoptosis (regulated cell death) is altered [4]. The disturbed flow present at the anastomosis has been implicated in the formation of IH and the link between hemodynamics and graft failure is via a complex cascade of events whereby biomechanical forces cause biological responses [5, 6]. For example, immediate early genes (IEG) such as c-fos, c-jun and egr-1 are involved in the signaling pathways for proliferation and apoptosis. When extracellular biomechanical stimuli (e.g. shear stress) cause the expression of IEG, their protein products translocate to the nucleus. These proteins regulate the expression of a number of genes implicated in cardiovascular disease including growth factors, adhesion molecules, proapoptotic substrates and coagulation factors [7–9]. Because IEG are involved in both proliferation and apoptosis, their expression may upset the normal balance between cell proliferation and apoptosis and could play a vital role in the IH formation in vascular bypass grafts.

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