Publication | Open Access
Coenzyme Q10 Decreases Basic Fibroblast Growth Factor (bFGF)-Induced Angiogenesis by Blocking ERK Activation
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2011
Year
Coenzyme Q10ImmunologyOxidative StressInflammationAngiogenesisBfgf-induced AngiogenesisFibroblast Growth FactorAtherosclerosisInhibitory ActivityCell SignalingBlocking Erk ActivationFibrosisVascular BiologyNeovascularizationVascular Endothelial Growth FactorPharmacologyCell BiologyTumor MicroenvironmentDevelopmental BiologyEndothelial DysfunctionMedicineExtracellular Matrix
Coenzyme Q10 (CoQ10) is an essential factor of the mitochondrial respiratory chain and has effective antioxidant properties. Therefore, CoQ10 has been used in a variety of clinical applications and used as a nutritional supplement to treat several human diseases. Here, we tested the effects of CoQ10 on angiogenesis stimulated by basic fibroblast growth factor (bFGF). CoQ10 significantly inhibited bFGF-induced angiogenesis in a mouse Matrigel plug and the sprouting of endothelial cells in rat aortic rings. In addition, CoQ10 decreased the ability of tube formation, migration, and invasion in endothelial cells. When CoQ10 was used to inhibit angiogenesis in endothelial cells, the expression of vascular endothelial growth factor (VEGF) and the phosphorylation of ERK were decreased. Taken together, these results indicate that CoQ10 is able to act as an antiangiogenic regulator, and its inhibitory activity is mediated by blocking an ERK-dependent pathway. This study suggests that CoQ10 may be used a therapeutic agent to decrease neovascularization in several diseases, including solid tumors.