NADPH oxidase and heart failure

Colin E. Murdoch; David J. Grieve; Alison C. Cave; Yee Hoo Looi; Ajay M. Shah

doi:10.1016/j.coph.2005.10.008

NADPH oxidase and heart failure

Colin E. Murdoch, David J. Grieve, Alison C. Cave, Yee Hoo Looi, Ajay M. Shah

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Abstract

Reactive oxygen species play important roles in the pathophysiology of chronic heart failure secondary to chronic left ventricular hypertrophy or myocardial infarction. Reactive oxygen species influence several components of the phenotype of the failing heart, including contractile function, interstitial fibrosis, endothelial dysfunction and myocyte hypertrophy. Recent studies implicate the production of reactive oxygen species by a family of NADPH oxidases in these effects. NADPH oxidases are activated in an isoform-specific manner by many pathophysiological stimuli and exert distinct downstream effects. Understanding NADPH oxidase activation and regulation, and their downstream effectors, could help to develop novel therapeutic targets.

Original language	English
Pages (from-to)	148-153
Number of pages	6
Journal	Current Opinion in Pharmacology
Volume	6
Issue number	2
DOIs	https://doi.org/10.1016/j.coph.2005.10.008
Publication status	Published - Apr 2006

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10.1016/j.coph.2005.10.008

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title = "NADPH oxidase and heart failure",

abstract = "Reactive oxygen species play important roles in the pathophysiology of chronic heart failure secondary to chronic left ventricular hypertrophy or myocardial infarction. Reactive oxygen species influence several components of the phenotype of the failing heart, including contractile function, interstitial fibrosis, endothelial dysfunction and myocyte hypertrophy. Recent studies implicate the production of reactive oxygen species by a family of NADPH oxidases in these effects. NADPH oxidases are activated in an isoform-specific manner by many pathophysiological stimuli and exert distinct downstream effects. Understanding NADPH oxidase activation and regulation, and their downstream effectors, could help to develop novel therapeutic targets.",

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AU - Murdoch, Colin E.

AU - Grieve, David J.

AU - Cave, Alison C.

AU - Looi, Yee Hoo

AU - Shah, Ajay M.

PY - 2006/4

Y1 - 2006/4

N2 - Reactive oxygen species play important roles in the pathophysiology of chronic heart failure secondary to chronic left ventricular hypertrophy or myocardial infarction. Reactive oxygen species influence several components of the phenotype of the failing heart, including contractile function, interstitial fibrosis, endothelial dysfunction and myocyte hypertrophy. Recent studies implicate the production of reactive oxygen species by a family of NADPH oxidases in these effects. NADPH oxidases are activated in an isoform-specific manner by many pathophysiological stimuli and exert distinct downstream effects. Understanding NADPH oxidase activation and regulation, and their downstream effectors, could help to develop novel therapeutic targets.

AB - Reactive oxygen species play important roles in the pathophysiology of chronic heart failure secondary to chronic left ventricular hypertrophy or myocardial infarction. Reactive oxygen species influence several components of the phenotype of the failing heart, including contractile function, interstitial fibrosis, endothelial dysfunction and myocyte hypertrophy. Recent studies implicate the production of reactive oxygen species by a family of NADPH oxidases in these effects. NADPH oxidases are activated in an isoform-specific manner by many pathophysiological stimuli and exert distinct downstream effects. Understanding NADPH oxidase activation and regulation, and their downstream effectors, could help to develop novel therapeutic targets.

U2 - 10.1016/j.coph.2005.10.008

DO - 10.1016/j.coph.2005.10.008

M3 - Article

SN - 1471-4892

VL - 6

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EP - 153

JO - Current Opinion in Pharmacology

JF - Current Opinion in Pharmacology

IS - 2

ER -

NADPH oxidase and heart failure

Abstract

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