Key result
Cyclophilin D inhibition rescues hypoxia-induced bioenergetic defects and improves cardiac function in neonatal mice.
Why the study?
Does CypD inhibition improve cardiac function and bioenergetics in neonatal mice exposed to hypoxia?
Does CypD inhibition improve cardiac function and bioenergetics in neonatal mice exposed to hypoxia?
Inhibition of cyclophilin D rescues cardiac dysfunction and bioenergetic defects caused by neonatal hypoxia in a murine model, identifying a potential therapeutic target for neonatal cardiac dysfunction.
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.
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Burris et al. (2026) studied Neonatal hypoxic cardiac dysfunction. Cyclophilin D (CypD) inhibition vs. Hypoxia without CypD inhibition was evaluated on Cardiac bioenergetics, myocyte maturation, and cardiac function. Cyclophilin D inhibition rescued most hypoxia-mediated defects in cardiac bioenergetics and myocyte maturation, and increased cardiac function in neonatal mice.
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