Key result
Neonatal hyperoxia drives broader transcriptional changes and stress pathway upregulation in the atrium versus ventricle.
Why the study?
Preterm infants often require oxygen at birth, but early exposure increases the risk of heart failure later in life.
May indicate heightened atrial vulnerability to neonatal hyperoxia; hypothesis-generating for arrhythmia risk studies in preterm survivors.
Preterm infants often require oxygen (hyperoxia) at birth, but early exposure increases the risk of heart failure later in life. Previously, we showed neonatal mice exposed to hyperoxia develop adult diastolic dysfunction and heart failure like preterm-born humans. In this study, RNA-sequencing reveals hyperoxia induces broader transcriptional changes in the atrium than ventricle, including upregulation of stress pathways and loss of superoxide dismutase 3 and extracellular matrix genes, highlighting the atrium's heightened vulnerability to hyperoxia.
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Yee et al. (2025) studied Neonatal hyperoxia. Neonatal hyperoxia was evaluated on Transcriptional changes in atrium vs ventricle. Neonatal hyperoxia induced broader transcriptional changes in the atrium than the ventricle, including upregulation of stress pathways, highlighting the atrium's heightened vulnerability.
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