Whole genome transcriptomics reveal distinct atrial versus ventricular responses to neonatal hyperoxia
Year: 2025
Type: article
Abstract: 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.
Authors: E. David Cohen, Min Yee, Kyle Roethlin, Irina Prelipcean, Eric M. Small, George A. Porter, Michael A. O’Reilly
Institutions: University of Rochester Medicine, University of Rochester
Language: English
Subfield: Pulmonary and Respiratory Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
Awards: Institutional Career Development Core, Dysregulation of common metabolic and transcriptional pathways in heart and lung fibrosis, G1402694829, G2172861667, G2720370934, G3541429436, Role of early life hyperoxia on mesenchymal stem cell fate: their impact on age related disease, G4236548530, G5084387240, G6249403818, G8026780026, Defining how neonatal hyperoxia causes pulmonary hypertension in adults, Environmental Agents as Modulators of Disease Processes, Intercalated disc-nuclear lamina coupling as a molecular substrate for arrhythmogenic cardiomyopathy, G992156545
OpenAlex ID: W4408186999