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Related Concept Videos

Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
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Differential Effects of Lipid-lowering Drugs in Modulating Morphology of Cholesterol Particles
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Statins have biphasic effects on angiogenesis.

Michael Weis1, Christopher Heeschen, Alec J Glassford

  • 1Stanford University School of Medicine, Division of Cardiovascular Medicine, Stanford, Calif 94305, USA.

Circulation
|February 13, 2002
PubMed
Summary
This summary is machine-generated.

Statins exhibit a dual effect on blood vessel formation (angiogenesis). Low doses promote it, while high doses inhibit it by affecting endothelial cells and vascular growth factors, independent of cholesterol levels.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Statins are HMG-CoA reductase inhibitors, impacting cholesterol and isoprenoid synthesis.
  • Isoprenoids regulate various cellular functions, including angiogenesis.
  • The effects of cerivastatin and atorvastatin on angiogenesis were investigated.

Purpose of the Study:

  • To investigate the dose-dependent effects of statins on angiogenesis.
  • To determine if these effects are lipid-dependent.
  • To explore the role of geranylgeranyl pyrophosphate in statin-mediated angiogenesis.

Main Methods:

  • In vitro studies using endothelial cells (proliferation, migration, differentiation).
  • In vivo studies in murine models of inflammation-induced angiogenesis.
  • Assessment of tumor growth and vascularization in a Lewis lung cancer model.

Main Results:

  • Low statin concentrations (0.005-0.01 µmol/L) enhanced endothelial cell functions.
  • High statin concentrations (0.05-1 µmol/L) inhibited angiogenesis, decreased vascular endothelial growth factor (VEGF), and increased endothelial apoptosis.
  • High-dose statins inhibited inflammation-induced angiogenesis and tumor growth in mice, effects reversed by geranylgeranyl pyrophosphate.

Conclusions:

  • HMG-CoA reductase inhibition has a biphasic, dose-dependent effect on angiogenesis.
  • Statin effects on angiogenesis are lipid-independent and linked to endothelial apoptosis and VEGF signaling.
  • Low therapeutic statin doses may be proangiogenic, while high doses are angiostatic, impacting geranylated proteins.