Does genetic reduction of vascular endothelial growth factor receptor 2 rescue aberrant angiogenesis caused by epsin deficiency?
Our results provide the first genetic demonstration that epsins function specifically to downregulate VEGFR2 by mediating activated VEGFR2 internalization and degradation and that genetic reduction of VEGFR2 level protects against excessive angiogenesis caused by epsin loss. Our findings indicate that epsins may be a potential therapeutic target in conditions in which tightly regulated angiogenesis is crucial, such as in diabetic wound healing and tumors.
Our results and comparisons with other available data show wide variation in the rate of CHD in diabetes, depending on the population and existing risk factors. Most individuals had a 10-year cumulative incidence >20%, but only those with multiple risk factors had a 10-year cumulative incidence that was equivalent to that of patients with CHD. Until more data are available, it may be prudent to consider targets based on the entire risk factor profile rather than just the presence of diabetes.