Aldosterone increases oxidant stress to impair guanylyl cyclase activity by cysteinyl thiol oxidation in vascular smooth muscle cells. - Wikidata - wikimedia - TriplyDB

Aldosterone increases oxidant stress to impair guanylyl cyclase activity by cysteinyl thiol oxidation in vascular smooth muscle cells.

Aldosterone increases oxidant stress to impair guanylyl cyclase activity by cysteinyl thiol oxidation in vascular smooth muscle cells.

http://www.wikidata.org/entity/Q43159940

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S-nitrosothiols and the S-nitrosoproteome of the cardiovascular system The role of the renin-angiotensin-aldosterone system in the pathobiology of pulmonary arterial hypertension (2013 Grover Conference series)Glutathione (GSH) and the GSH synthesis gene Gclm modulate plasma redox and vascular responses to acute diesel exhaust inhalation in mice Systems Pharmacology and Rational Polypharmacy: Nitric Oxide-Cyclic GMP Signaling Pathway as an Illustrative Example and Derivation of the General Case Reduction of aldosterone production improves renal oxidative stress and fibrosis in diabetic rats.Study design and rationale for investigating phosphodiesterase type 5 inhibition for the treatment of pulmonary hypertension due to chronic obstructive lung disease: the TADA-PHiLD (TADAlafil for Pulmonary Hypertension associated with chronic obstru Redox Pioneer: Professor Joseph Loscalzo.Systems analysis of oxidant stress in the vasculature Impact of glucose-6-phosphate dehydrogenase deficiency on the pathophysiology of cardiovascular disease.Aldosterone enhances IGF-I-mediated signaling and biological function in vascular smooth muscle cells New Developments in Platelet Cyclic Nucleotide Signalling: Therapeutic Implications.Aldosterone regulates vascular gene transcription via oxidative stress-dependent and -independent pathways.Genetic modifiers of hypertension in soluble guanylate cyclase α1-deficient mice Heme-assisted S-nitrosation desensitizes ferric soluble guanylate cyclase to nitric oxide Aldosterone inactivates the endothelin-B receptor via a cysteinyl thiol redox switch to decrease pulmonary endothelial nitric oxide levels and modulate pulmonary arterial hypertension.Plasma aldosterone levels are elevated in patients with pulmonary arterial hypertension in the absence of left ventricular heart failure: a pilot study Elevated pulmonary arterial and systemic plasma aldosterone levels associate with impaired cardiac reserve capacity during exercise in left ventricular systolic heart failure patients: A pilot study.Glutathione (GSH) and the GSH synthesis gene Gclm modulate vascular reactivity in mice.A nitric oxide/cysteine interaction mediates the activation of soluble guanylate cyclase.Thiol-Based Redox Modulation of Soluble Guanylyl Cyclase, the Nitric Oxide Receptor.Protein disulfide-isomerase interacts with soluble guanylyl cyclase via a redox-based mechanism and modulates its activity.Mineralocorticoid receptors in vascular function and disease.Obesity-related hypertension: epidemiology, pathophysiology, treatments, and the contribution of perivascular adipose tissue.Smooth muscle cell mineralocorticoid receptors: role in vascular function and contribution to cardiovascular disease.Direct contribution of vascular mineralocorticoid receptors to blood pressure regulation.Responses to reductive stress in the cardiovascular system.The Link Between Adipose Tissue Renin-Angiotensin-Aldosterone System Signaling and Obesity-Associated Hypertension.Antioxidant enzyme deficiencies and vascular disease.Adaptions to Hypoxia and Redox Stress: Essential Concepts Confounded by Misleading Terminology.Regulation of soluble guanylyl cyclase redox state by hydrogen sulfide.Systems biology: An emerging strategy for discovering novel pathogenetic mechanisms that promote cardiovascular disease.Guanylyl cyclase sensitivity to nitric oxide is protected by a thiol oxidation-driven interaction with thioredoxin-1.Rapid aldosterone signaling and vascular reactivity: relax or don't do it.Ebselen does not improve oxidative stress and vascular function in patients with diabetes: a randomized, crossover trial.Effects of hydrogen peroxide on relaxation through the NO/sGC/cGMP pathway in isolated rat iliac arteries.Distinct Myocardial Mechanisms Underlie Cardiac Dysfunction in Endotoxemic Male and Female Mice.Systems Biology Approaches to Redox Metabolism in Stress and Disease States.Structural and functional insights into the heme-binding domain of the human soluble guanylate cyclase α2 subunit and heterodimeric α2β1.Role of sulfhydryl-dependent dimerization of soluble guanylyl cyclase in relaxation of porcine coronary artery to nitric oxide.The Renin-Angiotensin-Aldosterone System as a Therapeutic Target in Late Injury Caused by Ischemia-Reperfusion.

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P2860

Aldosterone increases oxidant stress to impair guanylyl cyclase activity by cysteinyl thiol oxidation in vascular smooth muscle cells.

http://www.wikidata.org/entity/Q43159940

description

2009 nî lūn-bûn

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2009年の論文

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年學術文章

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2009年學術文章

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name

Aldosterone increases oxidant ...... vascular smooth muscle cells.

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Aldosterone increases oxidant ...... vascular smooth muscle cells.

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type

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Aldosterone increases oxidant ...... vascular smooth muscle cells.

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Aldosterone increases oxidant ...... vascular smooth muscle cells.

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Aldosterone increases oxidant ...... vascular smooth muscle cells.

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Aldosterone increases oxidant ...... vascular smooth muscle cells.

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Aldosterone increases oxidant ...... vascular smooth muscle cells.

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P2093

Annie Beuve

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Bradley A Maron

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Diane E Handy

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Jane A Leopold

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Shiow-Shih Tang

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Ying-Yi Zhang

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P2860

NO and CO differentially activate soluble guanylyl cyclase via a heme pivot-bend mechanism.

p22phox is a critical component of the superoxide-generating NADH/NADPH oxidase system and regulates angiotensin II-induced hypertrophy in vascular smooth muscle cells

In-gel digestion for mass spectrometric characterization of proteins and proteomes

Downregulation of soluble guanylyl cyclase in young and aging spontaneously hypertensive rats.

Widespread sulfenic acid formation in tissues in response to hydrogen peroxide.

Studying the structure and regulation of soluble guanylyl cyclase.

Aldosterone in congestive heart failure.

Targeting the heme-oxidized nitric oxide receptor for selective vasodilatation of diseased blood vessels

Deconstructing endothelial dysfunction: soluble guanylyl cyclase oxidation and the NO resistance syndrome.

Aldosteronism revisited: perspectives on less well-recognized actions of aldosterone.

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10.1074/JBC.M809460200

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12

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Joseph Loscalzo

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19141618

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