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Mechanism of the Sex Difference in Endothelial Dysfunction after Stroke

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Abstract

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.

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Acknowledgments

This work was supported by American Heart Association grant 10POST3630019 to CMD and by the Foundation for Anesthesia Education and Research (Rochester, MN, USA) FAER Research Fellowship Grant to SLF. The authors declare that they have no conflict of interest.

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Davis, C.M., Fairbanks, S.L. & Alkayed, N.J. Mechanism of the Sex Difference in Endothelial Dysfunction after Stroke. Transl. Stroke Res. 4, 381–389 (2013). https://doi.org/10.1007/s12975-012-0227-0

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