Key result
High glucose causes an uncoupling of VEGF with NO, which enhances endothelial cell proliferation via activation of the KDR-ERK1/2 pathway in bovine aortic endothelial cells.
Population
Bovine aortic endothelial cells (BAEC)
Comparison
High glucose or Nomega-nitro-l-arginine methyl… vs Control conditions (normal glucose, no L-NAME)
Design
Preclinical
Authors
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May link high glucose to diabetic endothelial proliferation; leaves open whether KDR-ERK1/2 targeting alters human outcomes.
High glucose uncouples VEGF from NO, leading to enhanced endothelial cell proliferation via the KDR-ERK1/2 pathway, providing a potential mechanism for diabetic vasculopathy.
Nakagawa et al. (2006) studied Diabetic vasculopathy. High glucose vs. Normal glucose was evaluated on Nitric oxide production and endothelial cell proliferation. High glucose causes an uncoupling of VEGF with NO, which enhances endothelial cell proliferation via activation of the KDR-ERK1/2 pathway in bovine aortic endothelial cells.
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