Mechanism of the Sex Difference in Endothelial Dysfunction after Stroke

Catherine M. Davis; Stacy L. Fairbanks; Nabil J. Alkayed

doi:10.1007/s12975-012-0227-0

Mechanism of the Sex Difference in Endothelial Dysfunction after Stroke

Catherine M. Davis, Stacy L. Fairbanks, Nabil J. Alkayed

Anesthesiology and Perioperative Medicine

Research output: Contribution to journal › Review article › peer-review

36 Scopus citations

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.

Original language	English (US)
Pages (from-to)	381-389
Number of pages	9
Journal	Translational Stroke Research
Volume	4
Issue number	4
DOIs	https://doi.org/10.1007/s12975-012-0227-0
State	Published - Aug 2013

Keywords

Brain
EET
Endothelia
Ischemia
Sexual dimorphism
sEH

ASJC Scopus subject areas

General Neuroscience
Clinical Neurology
Cardiology and Cardiovascular Medicine

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10.1007/s12975-012-0227-0

Cite this

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title = "Mechanism of the Sex Difference in Endothelial Dysfunction after Stroke",

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.",

keywords = "Brain, EET, Endothelia, Ischemia, Sexual dimorphism, sEH",

author = "Davis, {Catherine M.} and Fairbanks, {Stacy L.} and Alkayed, {Nabil J.}",

note = "Funding Information: 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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doi = "10.1007/s12975-012-0227-0",

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AU - Davis, Catherine M.

AU - Fairbanks, Stacy L.

AU - Alkayed, Nabil J.

N1 - Funding Information: 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.

PY - 2013/8

Y1 - 2013/8

N2 - 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.

AB - 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.

KW - Brain

KW - EET

KW - Endothelia

KW - Ischemia

KW - Sexual dimorphism

KW - sEH

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Mechanism of the Sex Difference in Endothelial Dysfunction after Stroke

Abstract

Keywords

ASJC Scopus subject areas

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