NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart. (Q34100612)

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:20713697%20AND%20SRC:MED&resulttype=core&format=json

10 February 2020

title

NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart (English)

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10 February 2020

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2

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10 February 2020

Michael D Schneider

5

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10 February 2020

Junichi Sadoshima

6

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10 February 2020

author name string

Junya Kuroda

1

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10 February 2020

Shouji Matsushima

3

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10 February 2020

Peiyong Zhai

4

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10 February 2020

language of work or name

English

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publication date

16 August 2010

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Proceedings of the National Academy of Sciences of the United States of America

10 February 2020

published in

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10 February 2020

volume

107

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10 February 2020

issue

35

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10 February 2020

page(s)

15565-15570

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Upregulation of Nox4 by hypertrophic stimuli promotes apoptosis and mitochondrial dysfunction in cardiac myocytes.

10 February 2020

cites work

1 reference

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Cardiac progenitor cell cycling stimulated by pim-1 kinase

5 July 2018

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Nox proteins in signal transduction

5 July 2018

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Quantitative analysis of redox-sensitive proteome with DIGE and ICAT.

5 July 2018

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A redox-dependent pathway for regulating class II HDACs and cardiac hypertrophy

5 July 2018

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Structure, regulation and evolution of Nox-family NADPH oxidases that produce reactive oxygen species

5 July 2018

1 reference

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A "reductionist" view of cardiomyopathy

5 July 2018

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The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology

5 July 2018

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Localizing NADPH oxidase-derived ROS.

5 July 2018

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NADPH oxidases in cardiovascular health and disease

5 July 2018

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NAD(P)H oxidase 4 mediates transforming growth factor-beta1-induced differentiation of cardiac fibroblasts into myofibroblasts

5 July 2018

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Disulfide relays and phosphorylative cascades: partners in redox-mediated signaling pathways

5 July 2018

1 reference

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Functional analysis of Nox4 reveals unique characteristics compared to other NADPH oxidases

5 July 2018

1 reference

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Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death

5 July 2018

1 reference

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Direct interaction of the novel Nox proteins with p22phox is required for the formation of a functionally active NADPH oxidase

5 July 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2932625

Redox-dependent modulation of aconitase activity in intact mitochondria

5 July 2018

1 reference

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Role of the mitochondrial permeability transition in myocardial disease

5 July 2018

1 reference

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A novel superoxide-producing NAD(P)H oxidase in kidney

5 July 2018

1 reference

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Reactive oxygen species (ROS)-induced ROS release: a new phenomenon accompanying induction of the mitochondrial permeability transition in cardiac myocytes

5 July 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2932625

Gene recombination in postmitotic cells. Targeted expression of Cre recombinase provokes cardiac-restricted, site-specific rearrangement in adult ventricular muscle in vivo.

5 July 2018

1 reference

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Activation of NADPH oxidase during progression of cardiac hypertrophy to failure

5 July 2018

1 reference

https://api.crossref.org/works/10.1073%2FPNAS.1002178107

Increased myocardial NADPH oxidase activity in human heart failure

21 January 2018

1 reference

https://api.crossref.org/works/10.1073%2FPNAS.1002178107

Nox4 as the major catalytic component of an endothelial NAD(P)H oxidase.

21 January 2018

1 reference

https://api.crossref.org/works/10.1073%2FPNAS.1002178107

Contrasting roles of NADPH oxidase isoforms in pressure-overload versus angiotensin II-induced cardiac hypertrophy

21 January 2018

1 reference

https://api.crossref.org/works/10.1073%2FPNAS.1002178107

Pressure overload-induced myocardial hypertrophy in mice does not require gp91phox

21 January 2018

1 reference

https://api.crossref.org/works/10.1073%2FPNAS.1002178107

Antioxidant changes in hypertrophied and failing guinea pig hearts

21 January 2018

1 reference

12 December 2020

Mitochondrial electron transport complex I is a potential source of oxygen free radicals in the failing myocardium

1 reference

12 December 2020

Redox regulation of growth and death in cardiac myocytes

1 reference

12 December 2020

Direct evidence for increased hydroxyl radicals originating from superoxide in the failing myocardium

1 reference

12 December 2020

Treatment with dimethylthiourea prevents left ventricular remodeling and failure after experimental myocardial infarction in mice: role of oxidative stress

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12 December 2020

Identifiers

DOI

10.1073/PNAS.1002178107

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:20713697%20AND%20SRC:MED&resulttype=core&format=json

10 February 2020

0 references

1 reference

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10 February 2020

PubMed publication ID

20713697

1 reference