For patients with advanced vascular disease, improving the efficacy of arteriogenesis may provide an alternative to invasive bypass surgery. Ren et al. discovered that shifting the balance between extracellular signal-regulated kinase (ERK)1/2 and phosphoinositide 3-kinase (PI3K)-Akt1, two crucial signaling arms that are activated by VEGF, stimulates arterial growth in mouse and zebrafish models of vascular disease. ERK1/2 is highly activated in growing arteries. This is in contrast to the PI3K-Akt1 pathway, which is thought to have an arterial stabilizing effect. In mice and zebrafish with decreased VEGF responsiveness and ERK1/2 activity, researchers restored ERK1/2 activation by downregulating PI3K-Akt1 activity or by introducing a constitutively activating ERK1/2. Both approaches stimulate arterial development. Inhibiting the PI3K-Akt1 pathway in an atherosclerotic mouse model effectively stimulated arterial formation. Thus, the PI3K-Akt1 pathway is a potential drug target for vascular disease.
RESEARCH HIGHLIGHT| 28 April 2010
Vascular disease: a novel molecular method for blood vessel formation
Online Issn: 1754-8411
Print Issn: 1754-8403
Dis Model Mech (2010) 3 (5-6): 256.
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Vascular disease: a novel molecular method for blood vessel formation. Dis Model Mech 28 April 2010; 3 (5-6): 256. doi:
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