ArticleAmerican journal of respiratory and critical care medicine2017
Vascular Endothelial Mitochondrial Function Predicts Death or Pulmonary Outcomes in Preterm Infants.
Article in American journal of respiratory and critical care medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 62 citations in OpenAlex.
- Alterations of endothelial cell bioenergetics in congenital diaphragmatic hernia.Pediatric research · 2026Article
- SLC25A28 Ameliorates Hyperoxic Lung Injury by Improving Mitochondrial Oxidative Phosphorylation in Alveolar Epithelial Cells.International journal of molecular sciences · 2026Article
- The evolving pathophysiology of bronchopulmonary dysplasia.Physiological reviews · 2026Review
- Mitochondrial quality control mechanisms as molecular targets for impaired lung development: from fetuses to neonates.Respiratory research · 2025Review
- Macrophage pyroptosis mediates hyperoxia-induced inflammatory lung injury in neonates.Frontiers in immunology · 2025Article
- Mitochondria as the central regulator of cell death in bronchopulmonary dysplasia.Frontiers in physiology · 2025Review
- Activated DRP1 promotes mitochondrial fission and induces glycolysis in ATII cells under hyperoxia.Respiratory research · 2024Article
- Aberrant PGC-1α signaling in a lamb model of persistent pulmonary hypertension of the newborn.Pediatric research · 2024Article
- Pathogenesis and Therapy of Hermansky-Pudlak Syndrome (HPS)-Associated Pulmonary Fibrosis.International journal of molecular sciences · 2024Review
- Decreased Liver Kinase B1 Expression and Impaired Angiogenesis in a Murine Model of Bronchopulmonary Dysplasia.American journal of respiratory cell and molecular biology · 2024Article
- [Role of reactive oxygen species/silent information regulator 1 in hyperoxia-induced bronchial epithelial cell injury].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024Article
- Predictive value of serum MED1 and PGC-1α for bronchopulmonary dysplasia in preterm infants.BMC pulmonary medicine · 2024Observational
- Visualization of the relationship between metabolism and lung diseases from the perspective of bibliometric analysis: research trends and future prospects.Frontiers in medicine · 2024Article
- Cord blood stem cell‑derived Angptl7 ameliorates the severity of bronchopulmonary dysplasia via anti‑inflammatory and proangiogenic effects.Molecular medicine reports · 2024Article
- L-citrulline attenuates lipopolysaccharide-induced inflammatory lung injury in neonatal rats.Pediatric research · 2023Article
- Prospective epigenome and transcriptome analyses of cord and peripheral blood from preterm infants at risk of bronchopulmonary dysplasia.Scientific reports · 2023Article
- Thyroid hormone modulates hyperoxic neonatal lung injury and mitochondrial function.JCI insight · 2023Article
- Neonatal intermittent hypoxia persistently impairs lung vascular development and induces long-term lung mitochondrial DNA damage.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Article
- Mesenchymal stem cell bioenergetics and apoptosis are associated with risk for bronchopulmonary dysplasia in extremely low birth weight infants.Scientific reports · 2022Article
- Cardiac Left Ventricle Mitochondrial Dysfunction After Neonatal Exposure to Hyperoxia: Relevance for Cardiomyopathy After Preterm Birth.Hypertension (Dallas, Tex. : 1979) · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
rationaleVascular endothelial mitochondrial dysfunction contributes to the pathogenesis of several oxidant stress-associated disorders. Oxidant stress is a major contributor to the pathogenesis of bronchopulmonary dysplasia (BPD), a chronic lung disease of prematurity that often leads to sequelae in adult survivors.
objectivesThis study was conducted to identify whether differences in mitochondrial bioenergetic function and oxidant generation in human umbilical vein endothelial cells (HUVECs) obtained from extremely preterm infants were associated with risk for BPD or death before 36 weeks postmenstrual age.
methodsHUVEC oxygen consumption and superoxide and hydrogen peroxide generation were measured in 69 infants. MEASUREMENTS AND MAIN
resultsCompared with HUVECs from infants who survived without BPD, HUVECs obtained from infants who developed BPD or died had a lower maximal oxygen consumption rate (mean ± SEM, 107 ± 8 vs. 235 ± 22 pmol/min/30,000 cells; P < 0.001), produced more superoxide after exposure to hyperoxia (mean ± SEM, 89,807 ± 16,616 vs. 162,706 ± 25,321 MitoSOX Red fluorescence units; P < 0.05), and released more hydrogen peroxide into the supernatant after hyperoxia exposure (mean ± SEM, 1,879 ± 278 vs. 842 ± 119 resorufin arbitrary fluorescence units; P < 0.001).
conclusionsOur results indicating that endothelial cells of premature infants who later develop BPD or die have impaired mitochondrial bioenergetic capacity and produce more oxidants at birth suggest that the vascular endothelial mitochondrial dysfunction seen at birth in these infants persists through their postnatal life and contributes to adverse pulmonary outcomes and increased early mortality.
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