ROS-induced ROS release in vascular biology: redox-redox signaling. - Wikidata - awgldk - TriplyDB

ROS-induced ROS release in vascular biology: redox-redox signaling.

ROS-induced ROS release in vascular biology: redox-redox signaling.

http://www.wikidata.org/entity/Q35314786

about

To breathe or not to breathe: the haematopoietic stem/progenitor cells dilemma Systemic and renal oxidative stress in the pathogenesis of hypertension: modulation of long-term control of arterial blood pressure by resveratrol Mitochondrial signaling: forwards, backwards, and in between Ceramide changes the mediator of flow-induced vasodilation from nitric oxide to hydrogen peroxide in the human microcirculation.Redox interplay between mitochondria and peroxisomes Mitochondria and arrhythmias.Antiplatelet effect of catechol is related to inhibition of cyclooxygenase, reactive oxygen species, ERK/p38 signaling and thromboxane A2 production Pleiotropic effects of the dipeptidylpeptidase-4 inhibitors on the cardiovascular system Nogo-B receptor modulates angiogenesis response of pulmonary artery endothelial cells through eNOS coupling Mitochondrial mechanisms in cerebral vascular control: shared signaling pathways with preconditioning.Emerging roles of mitochondria ROS in atherosclerotic lesions: causation or association?Glutathionylation of the L-type Ca2+ channel in oxidative stress-induced pathology of the heart.An acute rise in intraluminal pressure shifts the mediator of flow-mediated dilation from nitric oxide to hydrogen peroxide in human arterioles.Mitochondrial regulation of NADPH oxidase in hindlimb unweighting rat cerebral arteries.Sirtuin3 Dysfunction Is the Key Determinant of Skeletal Muscle Insulin Resistance by Angiotensin II Cross talk between NADPH oxidase and autophagy in pulmonary artery endothelial cells with intrauterine persistent pulmonary hypertension Key Role of ROS in the Process of 15-Lipoxygenase/15-Hydroxyeicosatetraenoiccid-Induced Pulmonary Vascular Remodeling in Hypoxia Pulmonary Hypertension.Role of reactive oxygen and nitrogen species in the vascular responses to inflammation.Activation of endothelial TRPV4 channels mediates flow-induced dilation in human coronary arterioles: role of Ca2+ entry and mitochondrial ROS signaling.Mitochondria and Oxidative Stress in the Cardiorenal Metabolic Syndrome.Measuring Redox Status of Melanoma Cells.Reactive oxygen species-targeted therapeutic interventions for atrial fibrillation.Reactive oxygen species-reducing strategies improve pulmonary arterial responses to nitric oxide in piglets with chronic hypoxia-induced pulmonary hypertension.Beyond the redox imbalance: Oxidative stress contributes to an impaired GLUT3 modulation in Huntington's disease TGF-β signalling and reactive oxygen species drive fibrosis and matrix remodelling in myxomatous mitral valves.Mitochondrial-localized NADPH oxidase 4 is a source of superoxide in angiotensin II-stimulated neurons.Molecular Mechanisms Linking Autonomic Dysfunction and Impaired Cardiac Contractility in Critical Illness Nox2 as a potential target of mitochondrial superoxide and its role in endothelial oxidative stress Role of mitochondrial oxidative stress in hypertension.Optogenetic control of ROS production.Therapeutic strategies to protect the immature newborn myocardium during resuscitation following asphyxia.ROS signalling between endothelial cells and cardiac cells.Crosstalk of mitochondria with NADPH oxidase via reactive oxygen and nitrogen species signalling and its role for vascular function.Central Nervous System Injury and Nicotinamide Adenine Dinucleotide Phosphate Oxidase: Oxidative Stress and Therapeutic Targets.MicroRNA hsa-let-7g targets lectin-like oxidized low-density lipoprotein receptor-1 expression and inhibits apoptosis in human smooth muscle cells.Transient Receptor Potential-Melastatin Channel Family Member 2: Friend or Foe Para-hydroxyphenylpyruvate inhibits the pro-inflammatory stimulation of macrophage preventing LPS-mediated nitro-oxidative unbalance and immunometabolic shift.NADPH oxidases in Parkinson's disease: a systematic review.From Physiological Redox Signalling to Oxidant Stress.Pathogenetic role of endothelial nitric oxide synthase uncoupling during lung ischaemia-reperfusion injury.

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P2860

ROS-induced ROS release in vascular biology: redox-redox signaling.

http://www.wikidata.org/entity/Q35314786

description

2011 nî lūn-bûn

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2011 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի հունիսին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

ROS-induced ROS release in vascular biology: redox-redox signaling.

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ROS-induced ROS release in vascular biology: redox-redox signaling.

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ROS-induced ROS release in vascular biology: redox-redox signaling.

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ROS-induced ROS release in vascular biology: redox-redox signaling.

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ROS-induced ROS release in vascular biology: redox-redox signaling.

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ROS-induced ROS release in vascular biology: redox-redox signaling.

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AJPHEART.01271.2010

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American Journal of Physiology - Heart and Circulatory Physiology

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ROS-induced ROS release in vascular biology: redox-redox signaling.

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David D Gutterman

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Natalya S Zinkevich

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P2860

Cytokine activation of nuclear factor kappa B in vascular smooth muscle cells requires signaling endosomes containing Nox1 and ClC-3

Reactive oxygen intermediates as apparently widely used messengers in the activation of the NF-kappa B transcription factor and HIV-1

Critical roles for p22phox in the structural maturation and subcellular targeting of Nox3

Oxidative stress and the use of antioxidants in diabetes: linking basic science to clinical practice.

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

H(2)O(2)-induced O(2) production by a non-phagocytic NAD(P)H oxidase causes oxidant injury

Endosomal NADPH oxidase regulates c-Src activation following hypoxia/reoxygenation injury

Peroxide-inducible Ets-1 mediates platelet-derived growth factor receptor-alpha gene transcription in vascular smooth muscle cells

Inducible platelet-derived growth factor D-chain expression by angiotensin II and hydrogen peroxide involves transcriptional regulation by Ets-1 and Sp1

High protonic potential actuates a mechanism of production of reactive oxygen species in mitochondria

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