Document Type
Article
Publication Date
4-24-2026
Abstract
Increased oxygen levels at birth regulate myocyte bioenergetic and structural maturation controlled by mitochondrial cyclophilin D (CypD). We evaluated mechanisms of neonatal hypoxic cardiac dysfunction by exposing neonatal mice to 12% oxygen and studied cardiac bioenergetics, myocyte maturation, and function. Hypoxia decreased the activity/assembly of electron transport chain complex I, uncoupled oxidative phosphorylation, increased proliferation, decreased differentiation, increased ventricular mass, and decreased cardiac function. CypD inhibition rescued most hypoxia-mediated effects and increased cardiac function. In conclusion, neonatal hypoxia alters cardiac bioenergetics, myocyte maturation, and cardiac function through CypD-dependent pathways, providing potential therapeutic targets for neonatal cardiac dysfunction.
Recommended Citation
Burris, Jonathan R.; Beutner, Gisela; Yee, Min; Simon, Bartholomew V.; Swartz, Michael F.; Boudreau, Kathryn B.; Cohen, Ethan D.; Kulkarni, Chaitanya A.; Hasan, Prottoy; Wang, Hongyue; de Mesy Bentley, Karen L.; Hajnóczky, György; Alfieris, George M.; Small, Eric M.; Brookes, Paul S.; O'Reilly, Michael A.; and Porter, George A., "Inhibition of Cyclophilin D Rescues Cardiac Function and Bioenergetic Defects Caused by Neonatal Hypoxia" (2026). Department of Pathology, Anatomy, and Cell Biology Faculty Papers. Paper 484.
https://jdc.jefferson.edu/pacbfp/484
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.
PubMed ID
42033870
Language
English
Comments
This article is the author's final published version in JACC: Basic to Translational Science, Volume 11, Issue 5, May 2026, Article Number 101544.
The published version is available at https://doi.org/10.1016/j.jacbts.2026.101544. Copyright © The Author(s).