Mechanism of the Sex Difference in Endothelial Dysfunction after Stroke

被引:43
作者
Davis, Catherine M. [1 ]
Fairbanks, Stacy L. [1 ]
Alkayed, Nabil J. [1 ]
机构
[1] Oregon Hlth & Sci Univ, Cerebrovasc Res Div, Dept Anesthesiol & Perioperat Med, Portland, OR 97239 USA
关键词
sEH; Ischemia; Endothelia; EET; Brain; Sexual dimorphism; SOLUBLE EPOXIDE HYDROLASE; EPOXYEICOSATRIENOIC ACID METABOLISM; ESTRADIOL-MEDIATED NEUROPROTECTION; ISCHEMIA-REPERFUSION INJURY; BLOOD-PRESSURE REGULATION; ESTROGEN-RECEPTOR-ALPHA; OBESE ZUCKER RATS; ARACHIDONIC-ACID; CEREBRAL-ISCHEMIA; THERAPEUTIC TARGET;
D O I
10.1007/s12975-012-0227-0
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Stroke, the number four cause of death in the USA, is a greatly debilitating event resulting from insufficient blood supply to the brain (cerebral ischemia). Endothelial dysfunction, primarily characterized by dampened endothelial-dependent vasodilation, is a major contributor to the development and outcome of stroke. This review discusses the role of soluble epoxide hydrolase, an enzyme responsible for the degradation of vasoprotective epoxyeicosatrienoic acids, in the context of the cerebral vasculature and its contribution to the sexual dimorphic nature of stroke.
引用
收藏
页码:381 / 389
页数:9
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