Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

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

Circulation research - 16 Apr 2010

Ago Tetsuro, Kuroda Junya, Pain Jayashree, Fu Cexiong, Li Hong, Sadoshima Junichi

Abstract excerpt

RATIONALE: NADPH oxidases are a major source of superoxide (O(2)(-)) in the cardiovascular system. The function of Nox4, a member of the Nox family of NADPH oxidases, in the heart is poorly understood. OBJECTIVE: The goal of this study was to elucidate the role of Nox4 in mediating oxidative stress and growth/death in the heart. METHODS AND RESULTS: Expression of Nox4 in the heart was increased in response to...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Aconitate Hydratase
Share to Cardiomegaly

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mitochondria, Heart

Share to Rotenone

Share to Superoxides

Share to Uncoupling Agents

Share to Ventricular Dysfunction, Left

Share to Ventricular Function, Left

Source

Open in PubMed Open full text

Identifiers

PMID: 20185797
DOI: 10.1161/CIRCRESAHA.109.213116
PMCID: PMC2855780

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Upregulation of Nox4 by hypertrophic stimuli promotes apoptosis and mitochondrial dysfunction in cardiac myocytes.PMID 20185797Read ↗

Pivotal role of miR-448 in the development of ROS-induced cardiomyopathy.Semantic proximity Read ↗

Skeletal muscle Nox4 knockout prevents and Nox2 knockout blunts loss of maximal diaphragm force in mice with heart failure with reduced ejection fractionSemantic proximity Read ↗

Alternative Splicing of NOX4 in the Failing Human HeartSemantic proximity Read ↗

Nox4 genetic inhibition in experimental hypertension and metabolic syndrome.Semantic proximity Read ↗

Cardiac-specific overexpression of catalase identifies hydrogen peroxide-dependent and -independent phases of myocardial remodeling and prevents the progression to overt heart failure in G(alpha)q-overexpressing transgenic mice.Semantic proximity Read ↗

Deficiency of NOX1/nicotinamide adenine dinucleotide phosphate, reduced form oxidase leads to pulmonary vascular remodeling.Semantic proximity Read ↗

NOX2 Is Critical to Endocardial to Mesenchymal Transition and Heart DevelopmentSemantic proximity Read ↗

Heart-Specific Knockout of the Mitochondrial Thioredoxin Reductase (Txnrd2) Induces Metabolic and Contractile Dysfunction in the Aging Myocardium.Semantic proximity Read ↗

Mitochondrial dysfunction and metabolic reprogramming induce macrophage pro-inflammatory phenotype switch and atherosclerosis progression in aging.Semantic proximity Read ↗

Aging triggers mitochondrial, endoplasmic reticulum, and metabolic stress responses in the heartSemantic proximity Read ↗

NADPH oxidase 4 induces cardiac arrhythmic phenotype in zebrafish.Semantic proximity Read ↗

Aging-Associated <i>Nox4</i> -Mediated Mitochondrial ROS and DNA Damage Promote Vascular Cell Reprogramming and Aortic Remodeling in Abdominal AneurysmsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.