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Cardiovascular Research 2004 63(1):11-21; doi:10.1016/j.cardiores.2004.02.009
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Control of vascular cell proliferation and migration by cyclin-dependent kinase signalling: new perspectives and therapeutic potential

Vicente Andrés*

Laboratory of Vascular Biology, Department of Molecular and Cellular Pathology and Therapy, Instituto de Biomedicina de Valencia, Consejo Superior de Investigaciones Cientificas, C/Jaime Roig 11, Valencia, 46010 Spain

*Tel.: +34-96-3391752; fax: +34-96-3391750. Email address: vandres{at}ibv.csic.es

Neointimal lesion development is a chronic inflammatory process that involves excessive cell proliferation and migration within the artery wall. Progression through the mammalian cell cycle requires the sequential activation of holoenzymes composed of a catalytic cyclin-dependent protein kinase (CDK) and a regulatory subunit named cyclin. Members of the family of CDK inhibitory proteins (CKIs) interact with and inhibit the activity of CDK/cyclins. Cell migration occurs predominantly at the G1/S phase of the cell cycle, and both CDKs and CKIs are among the molecular machines that coordinately regulate the cycling events that control cell proliferation and locomotion. The purpose of this review is to discuss the role of CDK/cyclins and CKIs in the regulation of vascular cell proliferation and migration and in the control of neointimal thickening. Pharmacological and gene therapy strategies targeting these cell cycle regulators for the treatment of cardiovascular disease will also be discussed.

KEYWORDS Vascular cell proliferation; Migration; CDK

Time for primary review 34 days


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