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Cardiovascular Research 2000 47(4):640-641; doi:10.1016/S0008-6363(00)00162-0
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

eNOS inhibition of proliferation: a role for p21Sdi1/Cip1/Waf1 and p27kip1

Cathy M. Holt*

Cardiovascular Research Group, Clinical Sciences Centre, Northern General Hospital, Sheffield S5 7AU, UK

* Corresponding author. Tel.: +44-114-271-4973; fax: +44-114-261-9587 c.holt@sheffield.ac.uk

Received 14 June 2000; accepted 26 June 2000

The first 10% of the full text of this article appears below.

See article by Sato et al. [12] (pages 697–706) in this issue.

It is over 10 years since NO donors were shown to reduce proliferation of vascular smooth muscle cells (VSMC) [1]. More recently, increase in vessel wall thickness and hyperplasia were shown to occur following ligation of the carotid artery in NO synthase (eNOS) knockout mice suggesting NO to be a negative regulator of vascular cell proliferation [2]. Due to the short half-life and limited solubility of NO, NO synthase (NOS) is often used as a way of enhancing local NO . . . [Full Text of this Article]


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