Increased Nox2 expression in human cardiomyocytes after acute myocardial infarction. - Wikidata - wikimedia - TriplyDB

Increased Nox2 expression in human cardiomyocytes after acute myocardial infarction.

Increased Nox2 expression in human cardiomyocytes after acute myocardial infarction.

http://www.wikidata.org/entity/Q35586674

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Identification and characterization of VPO1, a new animal heme-containing peroxidase Redox signaling regulated by electrophiles and reactive sulfur species NADPH oxidases in heart failure: poachers or gamekeepers?NOX2, p22phox and p47phox are targeted to the nuclear pore complex in ischemic cardiomyocytes colocalizing with local reactive oxygen species NOS1 induces NADPH oxidases and impairs contraction kinetics in aged murine ventricular myocytes.Redox regulation, NF-kappaB, and atrial fibrillation.Differential regulation of EHD3 in human and mammalian heart failure.Targeted antioxidant treatment decreases cardiac alternans associated with chronic myocardial infarction NADPH oxidases in cardiovascular disease: insights from in vivo models and clinical studies.Redox signalling and cardioprotection: translatability and mechanism Tissue kallikrein infusion prevents cardiomyocyte apoptosis, inflammation and ventricular remodeling after myocardial infarction.Nox enzymes, ROS, and chronic disease: an example of antagonistic pleiotropy.AAV-based RNAi silencing of NADPH oxidase gp91(phox) attenuates cold-induced cardiovascular dysfunction DNA hypermethylation of the NOX5 gene in fetal ventricular septal defect.NADPH oxidase-derived reactive oxygen species in cardiac pathophysiology Protection against ischemia-induced oxidative stress conferred by vagal stimulation in the rat heart: involvement of the AMPK-PKC pathway Angiotensin II (AT1) receptors and NADPH oxidase regulate Cl- current elicited by beta1 integrin stretch in rabbit ventricular myocytes Oxidative stress and redox signalling in cardiac hypertrophy and heart failure.Cardiomyocyte-specific overexpression of an active form of Rac predisposes the heart to increased myocardial stunning and ischemia-reperfusion injury NADPH oxidase 4 regulates cardiomyocyte differentiation via redox activation of c-Jun protein and the cis-regulation of GATA-4 gene transcription Inhibition of NADPH Oxidase Mediates Protective Effect of Cardiotonic Pills against Rat Heart Ischemia/Reperfusion Injury.NADPH oxidase contributes to coronary endothelial dysfunction in the failing heart NOX2 Antisense Attenuates Hypoxia-Induced Oxidative Stress and Apoptosis in Cardiomyocyte.Delivery of Nox2-NADPH oxidase siRNA with polyketal nanoparticles for improving cardiac function following myocardial infarction Angiotensin II-induced production of mitochondrial reactive oxygen species: potential mechanisms and relevance for cardiovascular disease.Cell-specific effects of Nox2 on the acute and chronic response to myocardial infarction.NADPH oxidase in brain injury and neurodegenerative disorders NADPH oxidases and cardiac remodelling.Opportunity nox: the future of NADPH oxidases as therapeutic targets in cardiovascular disease.Regulation of redox signalling by an electrophilic cyclic nucleotide.The "Goldilocks Zone" from a redox perspective-Adaptive vs. deleterious responses to oxidative stress in striated muscle.High-throughput screening identifies microRNAs that target Nox2 and improve function after acute myocardial infarction.Early NADPH oxidase-2 activation is crucial in phenylephrine-induced hypertrophy of H9c2 cells.The Pathophysiological Role of NOX2 in Hypertension and Organ Damage.A novel pathway of NADPH oxidase/vascular peroxidase 1 in mediating oxidative injury following ischemia-reperfusion.Role of NADPH oxidase in H9c2 cardiac muscle cells exposed to simulated ischaemia-reperfusion.Homocysteine-induced apoptosis in endothelial cells coincides with nuclear NOX2 and peri-nuclear NOX4 activity.Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury.The role of reactive oxygen species in the pathophysiology of cardiovascular diseases and the clinical significance of myocardial redox.The NADPH oxidase NOX2 as a novel biomarker for suicidality: evidence from human post mortem brain samples.

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P2860

Increased Nox2 expression in human cardiomyocytes after acute myocardial infarction.

http://www.wikidata.org/entity/Q35586674

description

2003 nî lūn-bûn

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2003年の論文

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2003年論文

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2003年論文

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2003年論文

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2003年論文

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2003年論文

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2003年论文

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2003年论文

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2003年论文

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name

Increased Nox2 expression in human cardiomyocytes after acute myocardial infarction.

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Increased Nox2 expression in human cardiomyocytes after acute myocardial infarction.

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type

label

Increased Nox2 expression in human cardiomyocytes after acute myocardial infarction.

@ast

Increased Nox2 expression in human cardiomyocytes after acute myocardial infarction.

@en

prefLabel

Increased Nox2 expression in human cardiomyocytes after acute myocardial infarction.

@ast

Increased Nox2 expression in human cardiomyocytes after acute myocardial infarction.

@en

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Journal of Clinical Pathology

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Increased Nox2 expression in human cardiomyocytes after acute myocardial infarction.

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P2093

Hack CE

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Krijnen PA

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Meijer CJ

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Meischl C

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Niessen HW

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Roos D

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Visser CA

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P2860

Cell transformation by the superoxide-generating oxidase Mox1

Cloning of two human thyroid cDNAs encoding new members of the NADPH oxidase family

Homologs of gp91phox: cloning and tissue expression of Nox3, Nox4, and Nox5

Molecular characterization and localization of the NAD(P)H oxidase components gp91-phox and p22-phox in endothelial cells

Novel gp91(phox) homologues in vascular smooth muscle cells : nox1 mediates angiotensin II-induced superoxide formation and redox-sensitive signaling pathways

Redox regulation of MAPK pathways and cardiac hypertrophy in adult rat cardiac myocyte.

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

Novel homologs of gp91phox.

Reactive oxygen species as mediators of signal transduction in cardiovascular disease.

Location of the epitope for 7D5, a monoclonal antibody raised against human flavocytochrome b558, to the extracellular peptide portion of primate gp91phox.

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