Vascular disease: a novel molecular method for blood vessel formation

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.