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

American Journal of Respiratory Cell and Molecular Biology

Volumn 40, Issue 5, 2009, Pages 511-518

  Ratner, Veniamin ^a   Starkov, Anatoly ^b   Matsiukevich, Dzmitry ^a   Polin, Richard A ^a   Ten, Vadim S ^a  

^a Och Spine at New York Presbyterian Hospitals   (United States)

^b WEILL CORNELL MEDICAL COLLEGE   (United States)

Author keywords

Bioenergetic failure; Bronchopulmonary dysplasia; Hyperoxia; Mitochondrial dysfunction

Indexed keywords

ADENOSINE DIPHOSPHATE; ADENOSINE TRIPHOSPHATE; COMPLEMENT COMPONENT C1; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE DEHYDROGENASE (UBIQUINONE);

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BIOENERGY; BREATHING RATE; CONTROLLED STUDY; DISORDERS OF MITOCHONDRIAL FUNCTIONS; HYPEROXIA; LUNG ALVEOLUS; LUNG DEVELOPMENT; LUNG DYSPLASIA; MITOCHONDRIAL RESPIRATION; MOUSE; NEWBORN; NONHUMAN; OXIDATIVE PHOSPHORYLATION; PREMATURITY; ANIMAL; C57BL MOUSE; CELL RESPIRATION; GROWTH, DEVELOPMENT AND AGING; METABOLISM; MITOCHONDRION; PATHOLOGY; PATHOPHYSIOLOGY; ULTRASTRUCTURE;

MUS;

ANIMALS; CELL RESPIRATION; ELECTRON TRANSPORT COMPLEX I; HYPEROXIA; MICE; MICE, INBRED C57BL; MITOCHONDRIA; PULMONARY ALVEOLI;

EID: 65349134323     PISSN: 10441549     EISSN: None     Source Type: Journal    
DOI: 10.1165/rcmb.2008-0341RC     Document Type: Article

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