Targeting NADPH oxidase decreases oxidative stress in the transgenic sickle cell mouse penis - Wikidata - awgldk - TriplyDB

Targeting NADPH oxidase decreases oxidative stress in the transgenic sickle cell mouse penis

Targeting NADPH oxidase decreases oxidative stress in the transgenic sickle cell mouse penis

http://www.wikidata.org/entity/Q36213625

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Sildenafil citrate-restored eNOS and PDE5 regulation in sickle cell mouse penis prevents priapism via control of oxidative/nitrosative stress Molecular pathophysiology of priapism: emerging targets Sustained nitric oxide (NO)-releasing compound reverses dysregulated NO signal transduction in priapism.Randomized controlled trial of sildenafil for preventing recurrent ischemic priapism in sickle cell disease.Transnitrosylation: A Factor in Nitric Oxide-Mediated Penile Erection.Ischaemic Priapism and Glucose-6-Phosphate Dehydrogenase Deficiency: A Mechanism of Increased Oxidative Stress?Nitrergic Mechanisms for Management of Recurrent Priapism Sildenafil promotes eNOS activation and inhibits NADPH oxidase in the transgenic sickle cell mouse penis.Ser/Thr protein kinase Bβ-NADPH oxidase 2 signaling in thromboinflammation.Mechanistic link between erectile dysfunction and systemic endothelial dysfunction in type 2 diabetic rats.Molecular analysis of erection regulatory factors in sickle cell disease associated priapism in the human penis.Beneficial Effect of the Nitric Oxide Donor Compound 3-(1,3-Dioxoisoindolin-2-yl)Benzyl Nitrate on Dysregulated Phosphodiesterase 5, NADPH Oxidase, and Nitrosative Stress in the Sickle Cell Mouse Penis: Implication for Priapism Treatment.Testosterone replacement in transgenic sickle cell mice controls priapic activity and upregulates PDE5 expression and eNOS activity in the penis.

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Targeting NADPH oxidase decreases oxidative stress in the transgenic sickle cell mouse penis

http://www.wikidata.org/entity/Q36213625

description

2012 nî lūn-bûn

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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2012年论文

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2012年论文

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name

Targeting NADPH oxidase decrea ...... sgenic sickle cell mouse penis

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Targeting NADPH oxidase decrea ...... sgenic sickle cell mouse penis

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Targeting NADPH oxidase decrea ...... sgenic sickle cell mouse penis

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Targeting NADPH oxidase decrea ...... sgenic sickle cell mouse penis

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Targeting NADPH oxidase decrea ...... sgenic sickle cell mouse penis

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J.1743-6109.2012.02798.X

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The Journal of Sexual Medicine

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Targeting NADPH oxidase decrea ...... sgenic sickle cell mouse penis

@en

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Arthur L Burnett

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Biljana Musicki

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Sena F Sezen

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Tongyun Liu

http://www.w3.org/2001/XMLSchema#string

P2860

Glutathione peroxidase 1 activity and cardiovascular events in patients with coronary artery disease

Excess adenosine in murine penile erectile tissues contributes to priapism via A2B adenosine receptor signaling

Regulation of endothelial nitric oxide synthase by tetrahydrobiopterin in vascular disease

Oxidation of tetrahydrobiopterin leads to uncoupling of endothelial cell nitric oxide synthase in hypertension

Establishment of a transgenic sickle-cell mouse model to study the pathophysiology of priapism.

Antisickling property of fetal hemoglobin enhances nitric oxide bioavailability and ameliorates organ oxidative stress in transgenic-knockout sickle mice.

Increased adenosine contributes to penile fibrosis, a dangerous feature of priapism, via A2B adenosine receptor signaling

Peroxynitrite induces destruction of the tetrahydrobiopterin and heme in endothelial nitric oxide synthase: transition from reversible to irreversible enzyme inhibition

Phosphodiesterase-5A dysregulation in penile erectile tissue is a mechanism of priapism.

Post-translational inactivation of endothelial nitric oxide synthase in the transgenic sickle cell mouse penis

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1980-1987

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scholarly article

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10.1111/J.1743-6109.2012.02798.X

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8

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22620981

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sickle-cell disease

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3435474

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