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Inhibition of Cyclophilin D Rescues Cardiac Function and Bioenergetic Defects Caused by Neonatal Hypoxia
Jonathan R Burris1, Gisela Beutner2, Min Yee3
1Division of Cardiology, Department of Pediatrics, University of Rochester Medical Center, Rochester, New York, USA; Division of Neonatology, Department of Pediatrics, University of Rochester Medical Center, Rochester, New York, USA.
JACC. Basic to Translational Science
|April 25, 2026
Summary
Neonatal hypoxia impairs heart function by disrupting energy production and cell development. Inhibiting mitochondrial cyclophilin D (CypD) improved cardiac function, suggesting CypD as a therapeutic target for infant heart issues.
Area of Science:
- Cardiology
- Neonatal Physiology
- Mitochondrial Biology
Background:
- Mitochondrial cyclophilin D (CypD) regulates cardiac development.
- Oxygen levels at birth are critical for myocyte maturation.
Purpose of the Study:
- To investigate the mechanisms of cardiac dysfunction in neonatal hypoxia.
- To evaluate the role of CypD in neonatal hypoxic cardiac dysfunction.
Main Methods:
- Neonatal mice were exposed to hypoxic conditions (12% oxygen).
- Cardiac bioenergetics, myocyte maturation, and function were assessed.
- The effects of CypD inhibition were studied.
Main Results:
- Hypoxia impaired electron transport chain complex I activity and oxidative phosphorylation.
- Hypoxia led to increased myocyte proliferation, decreased differentiation, increased ventricular mass, and reduced cardiac function.
- CypD inhibition ameliorated most hypoxia-induced effects and enhanced cardiac function.
Conclusions:
- Neonatal hypoxia negatively impacts cardiac bioenergetics, myocyte maturation, and function via CypD-dependent pathways.
- Targeting CypD presents a potential therapeutic strategy for neonatal cardiac dysfunction.
