ABSTRACT
Clinical studies indicate that 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase
inhibitor (statin) therapy has a cardiovascular protective activity that may result
from an improvement in endothelial function. Experimental studies have shown that
statins protect against ischaemia-reperfusion injury of the heart and stimulate the
growth of new blood vessels in ischemic limbs of normocholesterolemic animals. The
mechanisms underlying these serum lipid-independent effects of statins are not completely
understood, but there is increasing evidence that they improve endothelial function
through molecular mechanisms that mediate an increase in endothelium-derived nitric
oxide. Recent research has revealed a link between statins and the serine/threonine
protein kinase Akt that regulates multiple angiogenic processes in endothelial cells,
including the generation of nitrous oxide. In contrast to these data, it has also
been reported that higher doses of statins inhibit endothelial cell migration and
angiogenesis. Thus, further studies on the actions of statins may lead to the identification
of new pharmacological targets for the control of blood vessel growth.
KEYWORDS
Statin - angiogenesis - Akt - NO
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Kenneth WalshPh.D.
Molecular Cardiology/CVI, Boston University School of Medicine
715 Albany Street, W611
Boston, MA 02118