期刊
NATURE MEDICINE
卷 6, 期 9, 页码 1004-1010出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/79510
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资金
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [P01HD023681] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL050692] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR040197] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG015052] Funding Source: NIH RePORTER
- NHLBI NIH HHS [R01-HL50692, R01 HL050692-10] Funding Source: Medline
- NIAMS NIH HHS [R01 AR040197, R01 AR040197-11, R01-AR40197] Funding Source: Medline
- NIA NIH HHS [R01 AG015052, R01-AG15052, R01 AG015052-03] Funding Source: Medline
- NICHD NIH HHS [P01 HD023681] Funding Source: Medline
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.
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