Abstract
Statins promote the proliferation, migration, and survival of endothelial cells and bone marrow-derived endothelial progenitor cells (angioblasts) by stimulating the serine/threonine protein kinase Akt (also known as protein kinase B) pathway. Like vascular endothelial growth factor (VEGF), the statins promote angiogenesis and vasculogenesis. Therefore, Akt activation may explain some of the beneficial effects of the statins, including postnatal neovascularization.
MeSH terms
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Animals
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Cells, Cultured
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Cornea / drug effects
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Corneal Neovascularization
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Endothelial Growth Factors / physiology
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Endothelium, Vascular / cytology
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Endothelium, Vascular / drug effects*
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Humans
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Hypolipidemic Agents / pharmacology*
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Intercellular Signaling Peptides and Proteins / physiology
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Lymphokines / physiology
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Mice
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Neovascularization, Physiologic / drug effects*
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Protein Serine-Threonine Kinases / drug effects
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Proto-Oncogene Proteins c-akt
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Proto-Oncogene Proteins*
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RNA, Messenger / drug effects
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Rabbits
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Stem Cells / drug effects
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factors
Substances
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Endothelial Growth Factors
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Hypolipidemic Agents
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Intercellular Signaling Peptides and Proteins
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Lymphokines
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Proto-Oncogene Proteins
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RNA, Messenger
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factors
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AKT1 protein, human
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Protein Serine-Threonine Kinases
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Proto-Oncogene Proteins c-akt