Mitochondrial dysfunction contributes to alveolar developmental arrest in hyperoxia-exposed mice. - Wikidata - wikimedia - TriplyDB

Mitochondrial dysfunction contributes to alveolar developmental arrest in hyperoxia-exposed mice.

Mitochondrial dysfunction contributes to alveolar developmental arrest in hyperoxia-exposed mice.

http://www.wikidata.org/entity/Q40758514

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Early injury of the neonatal lung contributes to premature lung aging: a hypothesis Stem Cells and Their Mediators - Next Generation Therapy for Bronchopulmonary Dysplasia Animal Models, Learning Lessons to Prevent and Treat Neonatal Chronic Lung Disease Targeting mitochondrial dysfunction in lung diseases: emphasis on mitophagy Suppression of inflammatory cell trafficking and alveolar simplification by the heme oxygenase-1 product carbon monoxide A three-dimensional study of alveologenesis in mouse lung Reciprocal backcross mice confirm major loci linked to hyperoxic acute lung injury survival time.The Future of Bronchopulmonary Dysplasia: Emerging Pathophysiological Concepts and Potential New Avenues of Treatment.Epithelial ablation of Bcl-XL increases sensitivity to oxygen without disrupting lung development.Neonatal periostin knockout mice are protected from hyperoxia-induced alveolar simplication.Novel Flurometric Tool to Assess Mitochondrial Redox State of Isolated Perfused Rat Lungs after Exposure to Hyperoxia.Chemical compounds from anthropogenic environment and immune evasion mechanisms: potential interactions Activation of TNFR1 ectodomain shedding by mitochondrial Ca2+ determines the severity of inflammation in mouse lung microvessels.Hyperoxia decreases glycolytic capacity, glycolytic reserve and oxidative phosphorylation in MLE-12 cells and inhibits complex I and II function, but not complex IV in isolated mouse lung mitochondria.Differential responses of targeted lung redox enzymes to rat exposure to 60 or 85% oxygen.Coenzyme Q(1) as a probe for mitochondrial complex I activity in the intact perfused hyperoxia-exposed wild-type and Nqo1-null mouse lung.Mouse lung development and NOX1 induction during hyperoxia are developmentally regulated and mitochondrial ROS dependent.Role of glutathione in lung retention of 99mTc-hexamethylpropyleneamine oxime in two unique rat models of hyperoxic lung injury Mitochondrial DNA damage mediates hyperoxic dysmorphogenesis in rat fetal lung explants.The role of hyperoxia in the pathogenesis of experimental BPD.The circadian gene Rev-erbα improves cellular bioenergetics and provides preconditioning for protection against oxidative stress.Mechanical ventilation causes pulmonary mitochondrial dysfunction and delayed alveolarization in neonatal mice.Update in pediatric lung disease 2009.Emerging role of selective autophagy in human diseases.Mitochondrial dysfunction in inflammatory responses and cellular senescence: pathogenesis and pharmacological targets for chronic lung diseases.Mitochondrial dysfunction in alveolar and white matter developmental failure in premature infants.Methylenedioxymethamphetamine inhibits mitochondrial complex I activity in mice: a possible mechanism underlying neurotoxicity.Glycogen synthase kinase-3β/β-catenin signaling regulates neonatal lung mesenchymal stromal cell myofibroblastic differentiation.Mapping differential cellular protein response of mouse alveolar epithelial cells to multi-walled carbon nanotubes as a function of atomic layer deposition coating.Wood smoke exposure induces a decrease in respiration parameters and in the activity of respiratory complexes I and IV in lung mitochondria from guinea pigs.Attenuation of endoplasmic reticulum stress by caffeine ameliorates hyperoxia-induced lung injury.Differential Alterations of the Mitochondrial Morphology and Respiratory Chain Complexes during Postnatal Development of the Mouse Lung.Metabolic reprogramming in the pathogenesis of chronic lung diseases including BPD, COPD, and pulmonary fibrosis.Can We Understand the Pathobiology of Bronchopulmonary Dysplasia?Curcumin prevents paracetamol-induced liver mitochondrial alterations.The Potentials and Caveats of Mesenchymal Stromal Cell-Based Therapies in the Preterm Infant.

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Mitochondrial dysfunction contributes to alveolar developmental arrest in hyperoxia-exposed mice.

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American Journal of Respiratory Cell and Molecular Biology

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Mitochondrial dysfunction cont ...... rest in hyperoxia-exposed mice

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Dzmitry Matsiukevich

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Richard A Polin

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Vadim S Ten

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P2860

Early introduction of lipids to parenterally-fed preterm infants

Glutamine protects mitochondrial structure and function in oxygen toxicity.

Age-related alterations in oxidatively damaged proteins of mouse skeletal muscle mitochondrial electron transport chain complexes.

The molecular basis of lung morphogenesis.

The radial alveolar count method of Emery and Mithal: a reappraisal 2--intrauterine and early postnatal lung growth

Age-related increases in oxidatively damaged proteins of mouse kidney mitochondrial electron transport chain complexes

Progress in discovery and evaluation of treatments to prevent bronchopulmonary dysplasia.

Age-related alterations in oxidatively damaged proteins of mouse heart mitochondrial electron transport chain complexes.

Endothelial cell respiration is affected by the oxygen tension during shear exposure: role of mitochondrial peroxynitrite.

Chronic lung disease after premature birth.

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Anatoly Starkov

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