Review
Peroxisome proliferator activated receptor
: a potential
therapeutic target in the management of ischaemic heart
disease
J S Sidhu, J C Kaski
Coronary Artery
Disease Unit, Department of Cardiological Sciences, St George's
Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK
Correspondence to: Professor Kaski jkaski@sghms.ac.uk
Accepted 22 May 2001
| The first 150 words of the full text of this article appear below. |
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Introduction |
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In
recent years it has been established that inflammation has a pathogenic
role in atherosclerosis. Experimental studies have suggested that
altering transcription of proinflammatory genes can result in the
inhibition of atherosclerotic disease progression. Peroxisome
proliferator activated receptor
(PPAR
), a member of the nuclear
receptor superfamily of ligand activated transcription factors, is
highly expressed in several organs as well as in atherosclerotic plaques. Agonists of this receptor, such as rosiglitazone,
pioglitazone, and troglitazone, have insulin sensitising actions and
the former two agents are used clinically to treat type II diabetes.
PPAR
agonists can also inhibit the transcription of proinflammatory genes within plaques and have antithrombotic effects. Furthermore, PPAR
agonists have been shown to inhibit vascular smooth muscle cell
(VSMC) proliferation, which underlies restenosis after percutaneous coronary intervention. This article summarises our current
understanding of the role of PPAR
agonists in atherogenesis and
discusses their potential role in the treatment
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