Cell cycle regulation and control of angioplasty restenosis

The proliferative response of smooth muscle cells to injury remains the largest cause of clinical failure in interventions aimed at mitigating the effects of the atherosclerotic process. Contributing to this proliferative response are a number of factors including platelet and leukocyte adherence, transmigration, and activation with a concomitant release of a myriad of growth factors and remodelling of the extracellular matrix. The failure of attempts to modify this response by targeting single elements of the process is testimony to the redundancy of proliferative stimuli at work in the restenotic lesion. Therefore, interest has been directed towards the final common pathway of the proliferative vasculopathies, the cell cycle itself. The purpose of this chapter is to summarize recent attempts to control proliferation through interventions aimed at critical elements of the cell cycle, and to comment about how these interventions could be brought to bear in the clinical realm.