(Circulation. 2001;103:2414.)
© 2001 American Heart Association, Inc.
From Bench to Bedside |
Cell Cycle in Vasculoproliferative Diseases
Potential Interventions and Routes of Delivery
From the Division of Cardiology, University of Texas Medical Branch, Galveston, Texas (V.S.) and the Program in Molecular Cardiology, University of North Carolina at Chapel Hill (C.P.).
Correspondence to Cam Patterson, MD, University of North Carolina at Chapel Hill, 324 Burnett-Womack Bldg, Chapel Hill, NC 27599-7075. E-mail cpatters{at}med.unc.edu
Abstract—Atherosclerosis and restenosis of epicardial vessels are among the greatest challenges facing the clinical cardiologist, and phenotypic modulation and proliferation of smooth muscle cells are major components of the vasculoproliferative response. Proliferation is regulated by the interplay of regulatory proteins at checkpoints in the cell cycle that alter cellular growth. Activation of the cell cycle and the genetic control of its progression are final common pathways in this process. Investigators have postulated that cell-cycle inhibition using drugs and genetic or physical methods has the potential to reverse or prevent the vasculoproliferative process. The current challenge is to translate in vitro data demonstrating the efficacy of cell-cycle inhibition to clinical trials. At present, the steps that must be taken to meet this goal are (1) to design methods of delivery of these agents to specific sites, (2) to identify appropriate cellular targets to elicit cell-cycle arrest, and (3) to improve the therapeutic ratio by minimizing potential side effects. This review discusses current concepts of the cell cycle, target-regulating mechanisms, and possible interventions in vasculoproliferative diseases. We also discuss ongoing clinical trials that use antiproliferative agents in the hope of limiting the course of these diseases, as well as the promise that antiproliferative therapy holds in the coming decade.
Key Words: muscle, smooth • restenosis • gene therapy • pharmacology
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