Enhanced estradiol-induced vasorelaxation in aortas from type 2 diabetic mice may reflect a compensatory role of p38 MAPK-mediated eNOS activation.

Cardiovascular problems are a major cause of morbidity and mortality, mainly due to coronary artery disease and atherosclerosis, in type 2 diabetes mellitus. However, female gender is a protective factor in the development of, for example, atherosclerosis and hypertension. One of the female hormones, 17β-estradiol (E2), is known to protect against the cardiovascular injury resulting from endothelial dysfunction, but the mechanism by which it does so remains unknown.