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Nat Med. 2000 Sep;6(9):1004-10.

The HMG-CoA reductase inhibitor simvastatin activates the protein kinase Akt and promotes angiogenesis in normocholesterolemic animals.

Author information

1
Division of Cardiovascular Research, St. Elizabeth's Medical Center of Boston, Massachusetts 02135, USA.

Erratum in

  • Nat Med 2001 Jan;7(1):129.

Abstract

Recent studies suggest that statins can function to protect the vasculature in a manner that is independent of their lipid-lowering activity. We show here that statins rapidly activate the protein kinase Akt/PKB in endothelial cells. Accordingly, simvastatin enhanced phosphorylation of the endogenous Akt substrate endothelial nitric oxide synthase (eNOS), inhibited apoptosis and accelerated vascular structure formation in vitro in an Akt-dependent manner. Similar to vascular endothelial growth factor (VEGF) treatment, both simvastatin administration and enhanced Akt signaling in the endothelium promoted angiogenesis in ischemic limbs of normocholesterolemic rabbits. Therefore, activation of Akt represents a mechanism that can account for some of the beneficial side effects of statins, including the promotion of new blood vessel growth.

PMID:
10973320
PMCID:
PMC2828689
DOI:
10.1038/79510
[Indexed for MEDLINE]
Free PMC Article

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