Adenosine and arteriogenesis: promoter or suppressor?

This editorial refers to ‘Lack of ecto-5′-nucleotidase (CD73) promotes arteriogenesis’ by Y.C. Boring et al ., pp. 88-96, this issue. The principal therapeutic approach to atherosclerotic obstructive disease is to provide a sufficient blood flow to the jeopardized area perfused by the severely narrowed or occluded artery, which is accomplished by bypass grafting surgery, percutaneous transluminal intervention, and angiogenic therapy. Angiogenesis has been clearly separated into arteriogenesis and angiogenesis in a narrow sense in a rabbit hindlimb ischaemia model.1 Using the experimental model, Schaper et al. 2 established a conceptual framework of arteriogenesis.2 A pressure gradient across the collateral network increases the collateral blood flow, with resultant augmented fluid shear stress at the site of collateral vessels. Vascular endothelium activated by increased shear stress produces and releases monocyte chemotactic protein-1 (MCP-1) and adhesion molecules.3 Accumulated monocytes produce various angiogenic growth factors …