ArticleHypertension (Dallas, Tex. : 1979)2022
Cardiac Left Ventricle Mitochondrial Dysfunction After Neonatal Exposure to Hyperoxia: Relevance for Cardiomyopathy After Preterm Birth.
Article in Hypertension (Dallas, Tex. : 1979), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03261609 (Risk of Chronic Diseases in Young Adults Born Preterm), which is not on this map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Risk of Chronic Diseases in Young Adults Born Preterm: Relationship With Inflammation and Oxidative Stress Biomarkers.
Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Structural and Functional Abnormalities in the Preterm Heart: From Development to Adulthood.Journal of the American Heart Association · 2026Review
- Multiscale computational modeling of the cardiopulmonary consequences of postnatal hyperoxia with implications for preterm-born children.Biomechanics and modeling in mechanobiology · 2026Article
- Neonatal hyperoxia exposure does not exacerbate hypertension programmed by maternal obesity.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Article
- Cannabidiol Protects the Neonatal Mouse Heart from Hyperoxia-Induced Injury.International journal of molecular sciences · 2025Article
- Circulating Mitochondrial Open Reading Frame of the 12S Ribosomal RNA Type-c Is Higher in Acute Coronary Syndrome and Is a Prognostic Biomarker for Major Cardiac Events in Patients With Acute Myocardial Infarction: A Case-Control Study.Journal of the American Heart Association · 2025Article
- The vulnerable preterm heart: tale from the two chambers.American journal of physiology. Heart and circulatory physiology · 2025Article
- Mitochondrial DNA depletion syndrome and its cardiac complication.Frontiers in cardiovascular medicine · 2025Review
- The multifaceted role of mitochondria in cardiac function: insights and approaches.Cell communication and signaling : CCS · 2024Review
- Protective role of CXCR7 activation in neonatal hyperoxia-induced systemic vascular remodeling and cardiovascular dysfunction in juvenile rats.Scientific reports · 2023Article
- S14G-humanin confers cardioprotective effects against chronic adrenergic and pressure overload-induced heart failure in mice.Heliyon · 2023Article
- Disturbances of the Lung Glutathione System in Adult Guinea Pigs Following Neonatal Vitamin C or Cysteine Deficiency.Antioxidants (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundIndividuals born preterm present left ventricle changes and increased risk of cardiac diseases and heart failure. The pathophysiology of heart disease after preterm birth is incompletely understood. Mitochondria dysfunction is a hallmark of cardiomyopathy resulting in heart failure. We hypothesized that neonatal hyperoxia in rats, a recognized model simulating preterm birth conditions and resulting in oxygen-induced cardiomyopathy, induce left ventricle mitochondrial changes in juvenile rats. We also hypothesized that humanin, a mitochondrial-derived peptide, would be reduced in young adults born preterm.
methodsSprague-Dawley pups were exposed to room air (controls) or 80% O
resultsCompared with controls, oxygen-exposed rats showed smaller left ventricle mitochondria with disrupted integrity on electron microscopy, decreased oxidative phosphorylation, increased glycolysis markers, and reduced mitochondrial biogenesis and abundance. In oxygen-exposed rats, we observed lipid deposits, increased superoxide production (isolated cardiomyocytes), and reduced
conclusionsIn conclusion, neonatal hyperoxia impaired left ventricle mitochondrial structure and function in juvenile animals. Serum humanin level was reduced in preterm adults. This study suggests that preterm birth-related conditions entail left ventricle mitochondrial alterations that may underlie cardiac changes perpetuated into adulthood. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03261609.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.