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Atherosclerosis arises from an excessive fibroproliferative-inflammatory response to injury of the artery wall and typically evolves over decades (1). Smooth muscle cells play a central role in the development of atherosclerotic lesions. Their ability to migrate from the medial compartment of the artery wall to the intima, where they proliferate, accumulate lipid, and generate extracellular matrix, is key to the development of occlusive vascular lesions.  A common intervention for treating arterial blockage is percutaneous transluminal coronary angioplasty, in which an inflatable balloon is positioned at the site of arterial narrowing and used to physically disrupt the local atherosclerotic plaque. While angioplasty usually provides immediate symptomatic relief, its longer-term benefits are limited in a large proportion of cases (30–50% within 6 months) because the treated artery once again narrows at the site of inflation (2). This process, termed restenosis, involves elastic recoil, in the first instance, followed by extensive replication and remodeling — mainly by smooth muscle cells, which lay down matrix and eventually decrease luminal diameter at the site of ballooning. Most angioplasties are now performed in conjunction with the local deployment of metallic stents (3), which provide structural support in the reopened vessel by helping to prevent vascular recoil (4, 5).  Pharmacologic agents able to decrease the incidence of restenosis in human subjects are extremely limited, with antiplatelet glycoprotein IIb/IIIa receptor antagonists (inhibitors of platelet aggregation and thrombus formation) providing most utility. Intracoronary radiation, antioxidants, and growth factor antagonists have also shown promise as inhibitors of restenosis (6). The hunt for efficient inhibitors of restenosis remains an ongoing challenge. Here, I review the transcriptional control of specific genes that regulate smooth muscle cell biology, and I discuss the use of novel nucleic acid–based therapeutics that might be employed at the time of treatment to block restenosis over the long term.

Catalytic DNAs as potential therapeutic agents and sequence-specific molecular tools to dissect biological function