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• W2763734941 endingPage "2123" @default.
• W2763734941 startingPage "2123" @default.
• W2763734941 abstract "Several experimental studies have indicated that nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox) exert detrimental effects on ischemic brain tissue; Nox-knockout mice generally exhibit resistance to damage due to experimental stroke following middle cerebral artery occlusion (MCAO). Furthermore, our previous MCAO study indicated that infarct size and blood-brain barrier breakdown are enhanced in mice with pericyte-specific overexpression of Nox4, relative to levels observed in controls. However, it remains unclear whether Nox affects the stroke outcome directly by increasing oxidative stress at the site of ischemia, or indirectly by modifying physiological variables such as blood pressure or cerebral blood flow (CBF). Because of technical problems in the measurement of physiological variables and CBF, it is often difficult to address this issue in mouse models due to their small body size; in our previous study, we examined the effects of Nox activity on focal ischemic injury in a novel congenic rat strain: stroke-prone spontaneously hypertensive rats with loss-of-function in Nox. In this review, we summarize the current literature regarding the role of Nox in focal ischemic injury and discuss critical issues that should be considered when investigating Nox-related pathophysiology in animal models of stroke." @default.
• W2763734941 created "2017-10-20" @default.
• W2763734941 creator A5002376679 @default.
• W2763734941 creator A5050160011 @default.
• W2763734941 creator A5067341497 @default.
• W2763734941 creator A5091411173 @default.
• W2763734941 date "2017-10-11" @default.
• W2763734941 modified "2023-09-30" @default.
• W2763734941 title "NADPH Oxidase-Related Pathophysiology in Experimental Models of Stroke" @default.
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• W2763734941 doi "https://doi.org/10.3390/ijms18102123" @default.

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