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Nicotinamide adenine dinucleotide phosphate oxidase-4-dependent upregulation of nuclear factor erythroid-derived 2-like 2 protects the heart during chronic pressure overload

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Nicotinamide adenine dinucleotide phosphate oxidase-4-dependent upregulation of nuclear factor erythroid-derived 2-like 2 protects the heart during chronic pressure overload. / Smyrnias, Ioannis; Zhang, Xiaohong; Zhang, Min; Murray, Thomas V A; Brandes, Ralf P.; Schröder, Katrin; Brewer, Alison C.; Shah, Ajay M.

In: Hypertension, Vol. 65, No. 3, 04.03.2015, p. 547-553.

Research output: Contribution to journalArticle

Harvard

Smyrnias, I, Zhang, X, Zhang, M, Murray, TVA, Brandes, RP, Schröder, K, Brewer, AC & Shah, AM 2015, 'Nicotinamide adenine dinucleotide phosphate oxidase-4-dependent upregulation of nuclear factor erythroid-derived 2-like 2 protects the heart during chronic pressure overload', Hypertension, vol. 65, no. 3, pp. 547-553. https://doi.org/10.1161/HYPERTENSIONAHA.114.04208

APA

Smyrnias, I., Zhang, X., Zhang, M., Murray, T. V. A., Brandes, R. P., Schröder, K., ... Shah, A. M. (2015). Nicotinamide adenine dinucleotide phosphate oxidase-4-dependent upregulation of nuclear factor erythroid-derived 2-like 2 protects the heart during chronic pressure overload. Hypertension, 65(3), 547-553. https://doi.org/10.1161/HYPERTENSIONAHA.114.04208

Vancouver

Smyrnias I, Zhang X, Zhang M, Murray TVA, Brandes RP, Schröder K et al. Nicotinamide adenine dinucleotide phosphate oxidase-4-dependent upregulation of nuclear factor erythroid-derived 2-like 2 protects the heart during chronic pressure overload. Hypertension. 2015 Mar 4;65(3):547-553. https://doi.org/10.1161/HYPERTENSIONAHA.114.04208

Author

Smyrnias, Ioannis ; Zhang, Xiaohong ; Zhang, Min ; Murray, Thomas V A ; Brandes, Ralf P. ; Schröder, Katrin ; Brewer, Alison C. ; Shah, Ajay M. / Nicotinamide adenine dinucleotide phosphate oxidase-4-dependent upregulation of nuclear factor erythroid-derived 2-like 2 protects the heart during chronic pressure overload. In: Hypertension. 2015 ; Vol. 65, No. 3. pp. 547-553.

Bibtex Download

@article{5d96bd3cd5dc4d759dc12f89402be0db,
title = "Nicotinamide adenine dinucleotide phosphate oxidase-4-dependent upregulation of nuclear factor erythroid-derived 2-like 2 protects the heart during chronic pressure overload",
abstract = "The transcription factor nuclear factor erythroid-derived 2-like 2 (Nrf2) controls a network of cytoprotective genes. Neither how Nrf2 is activated in the heart under hemodynamic overload nor its role and mechanism of action are known. This study aimed to investigate the activation and role of Nrf2 during chronic cardiac pressure overload. We first compared the responses of Nrf2-/- mice and wild-type littermates to chronic pressure overload. Hearts of Nrf2-/- mice showed impaired antioxidant gene expression, increased hypertrophy, and worse function compared with those of wild-type littermates after overload. Hearts of Nrf2-/- mice had increased mitochondrial DNA damage, a caspase 8/BH3-interacting domain death agonist-related cleavage of mitochondrial apoptosis-inducing factor, nuclear DNA damage, and cell death. Nrf2 activation was under the control of the endogenous reactive oxygen species-generating enzyme nicotinamide adenine dinucleotide phosphate oxidase-4, both in vivo and in vitro. In mice with cardiac-specific overexpression of nicotinamide adenine dinucleotide phosphate oxidase-4, Nrf2 deletion significantly attenuated their protective phenotype during chronic pressure overload. This study identifies nicotinamide adenine dinucleotide phosphate oxidase-4-dependent upregulation of Nrf2 as an important endogenous protective pathway that limits mitochondrial damage and apoptosis-inducing factor-related cell death in the heart under hemodynamic overload.",
keywords = "cell death, Nfe2l2 protein, mouse, Nox4 protein, mouse, oxidative stress",
author = "Ioannis Smyrnias and Xiaohong Zhang and Min Zhang and Murray, {Thomas V A} and Brandes, {Ralf P.} and Katrin Schr{\"o}der and Brewer, {Alison C.} and Shah, {Ajay M.}",
year = "2015",
month = "3",
day = "4",
doi = "10.1161/HYPERTENSIONAHA.114.04208",
language = "English",
volume = "65",
pages = "547--553",
journal = "Hypertension",
issn = "0194-911X",
publisher = "American Heart Association, Inc.",
number = "3",

}

RIS (suitable for import to EndNote) Download

TY - JOUR

T1 - Nicotinamide adenine dinucleotide phosphate oxidase-4-dependent upregulation of nuclear factor erythroid-derived 2-like 2 protects the heart during chronic pressure overload

AU - Smyrnias, Ioannis

AU - Zhang, Xiaohong

AU - Zhang, Min

AU - Murray, Thomas V A

AU - Brandes, Ralf P.

AU - Schröder, Katrin

AU - Brewer, Alison C.

AU - Shah, Ajay M.

PY - 2015/3/4

Y1 - 2015/3/4

N2 - The transcription factor nuclear factor erythroid-derived 2-like 2 (Nrf2) controls a network of cytoprotective genes. Neither how Nrf2 is activated in the heart under hemodynamic overload nor its role and mechanism of action are known. This study aimed to investigate the activation and role of Nrf2 during chronic cardiac pressure overload. We first compared the responses of Nrf2-/- mice and wild-type littermates to chronic pressure overload. Hearts of Nrf2-/- mice showed impaired antioxidant gene expression, increased hypertrophy, and worse function compared with those of wild-type littermates after overload. Hearts of Nrf2-/- mice had increased mitochondrial DNA damage, a caspase 8/BH3-interacting domain death agonist-related cleavage of mitochondrial apoptosis-inducing factor, nuclear DNA damage, and cell death. Nrf2 activation was under the control of the endogenous reactive oxygen species-generating enzyme nicotinamide adenine dinucleotide phosphate oxidase-4, both in vivo and in vitro. In mice with cardiac-specific overexpression of nicotinamide adenine dinucleotide phosphate oxidase-4, Nrf2 deletion significantly attenuated their protective phenotype during chronic pressure overload. This study identifies nicotinamide adenine dinucleotide phosphate oxidase-4-dependent upregulation of Nrf2 as an important endogenous protective pathway that limits mitochondrial damage and apoptosis-inducing factor-related cell death in the heart under hemodynamic overload.

AB - The transcription factor nuclear factor erythroid-derived 2-like 2 (Nrf2) controls a network of cytoprotective genes. Neither how Nrf2 is activated in the heart under hemodynamic overload nor its role and mechanism of action are known. This study aimed to investigate the activation and role of Nrf2 during chronic cardiac pressure overload. We first compared the responses of Nrf2-/- mice and wild-type littermates to chronic pressure overload. Hearts of Nrf2-/- mice showed impaired antioxidant gene expression, increased hypertrophy, and worse function compared with those of wild-type littermates after overload. Hearts of Nrf2-/- mice had increased mitochondrial DNA damage, a caspase 8/BH3-interacting domain death agonist-related cleavage of mitochondrial apoptosis-inducing factor, nuclear DNA damage, and cell death. Nrf2 activation was under the control of the endogenous reactive oxygen species-generating enzyme nicotinamide adenine dinucleotide phosphate oxidase-4, both in vivo and in vitro. In mice with cardiac-specific overexpression of nicotinamide adenine dinucleotide phosphate oxidase-4, Nrf2 deletion significantly attenuated their protective phenotype during chronic pressure overload. This study identifies nicotinamide adenine dinucleotide phosphate oxidase-4-dependent upregulation of Nrf2 as an important endogenous protective pathway that limits mitochondrial damage and apoptosis-inducing factor-related cell death in the heart under hemodynamic overload.

KW - cell death

KW - Nfe2l2 protein, mouse

KW - Nox4 protein, mouse

KW - oxidative stress

UR - http://www.scopus.com/inward/record.url?scp=84924227907&partnerID=8YFLogxK

U2 - 10.1161/HYPERTENSIONAHA.114.04208

DO - 10.1161/HYPERTENSIONAHA.114.04208

M3 - Article

C2 - 25534702

AN - SCOPUS:84924227907

VL - 65

SP - 547

EP - 553

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 3

ER -

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