The triterpenoid CDDO-imidazolide confers potent protection against hyperoxic acute lung injury in mice. - Wikidata - awgldk - TriplyDB

The triterpenoid CDDO-imidazolide confers potent protection against hyperoxic acute lung injury in mice.

The triterpenoid CDDO-imidazolide confers potent protection against hyperoxic acute lung injury in mice.

http://www.wikidata.org/entity/Q37413347

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The triterpenoid CDDO-Me inhibits bleomycin-induced lung inflammation and fibrosis New synthetic triterpenoids: potent agents for prevention and treatment of tissue injury caused by inflammatory and oxidative stress Stress-activated cap'n'collar transcription factors in aging and human disease Noblesse oblige: NRF2 functions in the airways.Proteomic analysis shows synthetic oleanane triterpenoid binds to mTOR Triterpenoids CDDO-ethyl amide and CDDO-trifluoroethyl amide improve the behavioral phenotype and brain pathology in a transgenic mouse model of Huntington's disease Regulation of notch1 signaling by nrf2: implications for tissue regeneration Targeting maladaptive glutathione responses in lung disease.CDDO-imidazolide induces DNA damage, G2/M arrest and apoptosis in BRCA1-mutated breast cancer cells Update on acute lung injury and critical care medicine 2009.Nrf2 reduces allergic asthma in mice through enhanced airway epithelial cytoprotective function Thioredoxin reductase inhibition elicits Nrf2-mediated responses in Clara cells: implications for oxidant-induced lung injury Synthetic oleanane triterpenoids: multifunctional drugs with a broad range of applications for prevention and treatment of chronic disease.Respiratory syncytial virus infection: mechanisms of redox control and novel therapeutic opportunities Hydrogen gas reduces hyperoxic lung injury via the Nrf2 pathway in vivo Role of Nrf2 and Autophagy in Acute Lung Injury The Nrf2 triterpenoid activator, CDDO-imidazolide, protects kidneys from ischemia-reperfusion injury in mice.Association of Nrf2 with airway pathogenesis: lessons learned from genetic mouse models.Thioredoxin Reductase Inhibition Attenuates Neonatal Hyperoxic Lung Injury and Enhances Nuclear Factor E2-Related Factor 2 Activation.The Keap1-Nrf2-ARE Pathway As a Potential Preventive and Therapeutic Target: An Update.The triterpenoid CDDO-imidazolide ameliorates mouse liver ischemia-reperfusion injury through activating the Nrf2/HO-1 pathway enhanced autophagy.Time Course Expression Analysis of 1[2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oyl]imidazole Induction of Cytoprotection in Human Endothelial Cells.ROS Signaling in the Pathogenesis of Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS).Anti-inflammatory efficacy of dexamethasone and Nrf2 activators in the CNS using brain slices as a model of acute injury.Aurothioglucose Does Not Improve Alveolarization or Elicit Sustained Nrf2 Activation in C57Bl/6 Models of Bronchopulmonary Dysplasia.

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The triterpenoid CDDO-imidazolide confers potent protection against hyperoxic acute lung injury in mice.

http://www.wikidata.org/entity/Q37413347

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 13 August 2009

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

The triterpenoid CDDO-imidazol ...... xic acute lung injury in mice.

@en

The triterpenoid CDDO-imidazol ...... xic acute lung injury in mice.

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type

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The triterpenoid CDDO-imidazol ...... xic acute lung injury in mice.

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The triterpenoid CDDO-imidazol ...... xic acute lung injury in mice.

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The triterpenoid CDDO-imidazol ...... xic acute lung injury in mice.

@en

The triterpenoid CDDO-imidazol ...... xic acute lung injury in mice.

@nl

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RCCM.200905-0670OC

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American Journal of Respiratory and Critical Care Medicine

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The triterpenoid CDDO-imidazol ...... xic acute lung injury in mice.

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Masayuki Yamamoto

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Melinda S Yates

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Michael B Sporn

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Narsa M Reddy

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Paul M Hassoun

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Sekhar P Reddy

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Steven R Kleeberger

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Thomas W Kensler

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Vegiraju Suryanaraya

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P2860

Oxidative stress sensor Keap1 functions as an adaptor for Cul3-based E3 ligase to regulate proteasomal degradation of Nrf2

Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network

Direct evidence that sulfhydryl groups of Keap1 are the sensors regulating induction of phase 2 enzymes that protect against carcinogens and oxidants

An Nrf2/small Maf heterodimer mediates the induction of phase II detoxifying enzyme genes through antioxidant response elements

The acute respiratory distress syndrome

Regulatory mechanisms controlling gene expression mediated by the antioxidant response element

A genetic mouse model to investigate hyperoxic acute lung injury survival.

Disruption of Nrf2 impairs the resolution of hyperoxia-induced acute lung injury and inflammation in mice

DNA damage and cell cycle checkpoints in hyperoxic lung injury: braking to facilitate repair.

Oxidative stress and lung inflammation in airways disease.

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867-874

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10.1164/RCCM.200905-0670OC

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