Mechanisms of diesel-induced endothelial nitric oxide synthase dysfunction in coronary arterioles - Wikidata - awgldk - TriplyDB

Mechanisms of diesel-induced endothelial nitric oxide synthase dysfunction in coronary arterioles

Mechanisms of diesel-induced endothelial nitric oxide synthase dysfunction in coronary arterioles

http://www.wikidata.org/entity/Q28385682

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MMP-9-dependent serum-borne bioactivity caused by multiwalled carbon nanotube exposure induces vascular dysfunction via the CD36 scavenger receptor Nanoparticle inhalation alters systemic arteriolar vasoreactivity through sympathetic and cyclooxygenase-mediated pathways Intravenous and gastric cerium dioxide nanoparticle exposure disrupts microvascular smooth muscle signaling Potential Harmful Effects of PM2.5 on Occurrence and Progression of Acute Coronary Syndrome: Epidemiology, Mechanisms, and Prevention Measures Pulmonary instillation of MWCNT increases lung permeability, decreases gp130 expression in the lungs, and initiates cardiovascular IL-6 transsignaling Pulmonary instillation of multi-walled carbon nanotubes promotes coronary vasoconstriction and exacerbates injury in isolated hearts Glutathione (GSH) and the GSH synthesis gene Gclm modulate plasma redox and vascular responses to acute diesel exhaust inhalation in mice Ozone Inhalation Impairs Coronary Artery Dilation via Intracellular Oxidative Stress: Evidence for Serum-Borne Factors as Drivers of Systemic Toxicity Engine exhaust particulate and gas phase contributions to vascular toxicity Comparative plasma proteomic studies of pulmonary TiO2 nanoparticle exposure in rats using liquid chromatography tandem mass spectrometry Formation of vascular S-nitrosothiols and plasma nitrates/nitrites following inhalation of diesel emissions Xenobiotic particle exposure and microvascular endpoints: a call to arms Vascular endothelium as a target of diesel particulate matter-associated toxicants Oxidative stress and air pollution exposure In utero exposure to diesel exhaust air pollution promotes adverse intrauterine conditions, resulting in weight gain, altered blood pressure, and increased susceptibility to heart failure in adult mice.Features of microglia and neuroinflammation relevant to environmental exposure and neurotoxicity.Combustion-derived nanoparticulate induces the adverse vascular effects of diesel exhaust inhalation.DIESEL particulate exposed macrophages alter endothelial cell expression of eNOS, iNOS, MCP1, and glutathione synthesis genes Endothelial inflammatory transcriptional responses to an altered plasma exposome following inhalation of diesel emissions NFAT is required for spontaneous pulmonary hypertension in superoxide dismutase 1 knockout mice.CD36 mediates endothelial dysfunction downstream of circulating factors induced by O3 exposure.In utero and early life exposure to diesel exhaust air pollution increases adult susceptibility to heart failure in mice.Intermittent hypoxia-induced increases in reactive oxygen species activate NFATc3 increasing endothelin-1 vasoconstrictor reactivity.Endothelial responses of the alveolar barrier in vitro in a dose-controlled exposure to diesel exhaust particulate matter.Composition of air pollution particles and oxidative stress in cells, tissues, and living systems.From particles to patients: oxidative stress and the cardiovascular effects of air pollution.Salt, Angiotensin II, Superoxide, and Endothelial Function.Causation by Diesel Exhaust Particles of Endothelial Dysfunctions in Cytotoxicity, Pro-inflammation, Permeability, and Apoptosis Induced by ROS Generation.Atherosclerosis and vasomotor dysfunction in arteries of animals after exposure to combustion-derived particulate matter or nanomaterials.Oxidative Stress and Cardiovascular Risk: Obesity, Diabetes, Smoking, and Pollution: Part 3 of a 3-Part Series.Pulmonary exposure to particles from diesel exhaust, urban dust or single-walled carbon nanotubes and oxidatively damaged DNA and vascular function in apoE(-/-) mice.Inhalation of diesel exhaust does not exacerbate cardiac hypertrophy or heart failure in two mouse models of cardiac hypertrophy.Lipophilic components of diesel exhaust particles induce pro-inflammatory responses in human endothelial cells through AhR dependent pathway(s).

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Mechanisms of diesel-induced endothelial nitric oxide synthase dysfunction in coronary arterioles

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2011 թուականի Յունուարին հրատարակուած գիտական յօդուած

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Mechanisms of diesel-induced e ...... unction in coronary arterioles

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Mechanisms of diesel-induced e ...... unction in coronary arterioles

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Mechanisms of diesel-induced e ...... unction in coronary arterioles

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Mechanisms of diesel-induced e ...... unction in coronary arterioles

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Mechanisms of diesel-induced e ...... unction in coronary arterioles

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Mechanisms of diesel-induced e ...... unction in coronary arterioles

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Mechanisms of diesel-induced e ...... unction in coronary arterioles

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Benjimen R Walker

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Matthew J Campen

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Michael L Paffett

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Nancy L Kanagy

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Olan Jackson-Weaver

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Tom W Cherng

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P2860

Pulmonary nanoparticle exposure disrupts systemic microvascular nitric oxide signaling

Systemic microvascular dysfunction and inflammation after pulmonary particulate matter exposure

Tetrahydrobiopterin biosynthesis, regeneration and functions

Association of fine particulate matter from different sources with daily mortality in six U.S. cities

Association of air pollution with increased incidence of ventricular tachyarrhythmias recorded by implanted cardioverter defibrillators

Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method

Nitric oxide synthases: structure, function and inhibition

Persistent endothelial dysfunction in humans after diesel exhaust inhalation

Diffusion of peroxynitrite into the human platelet inhibits cyclooxygenase via nitration of tyrosine residues

Impairment of NO-dependent relaxation in intralobar pulmonary arteries: comparison of urban particulate matter and manufactured nanoparticles

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10.1289/EHP.1002286

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119

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3018507

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