Key result
Monocrotaline-induced hypertrophic right ventricular cardiomyocytes had larger cytosolic and mitochondrial Ca2+ transients and increased mitochondrial protein abundance compared to saline controls.
Why the study?
In pulmonary artery hypertension, alterations in cytosolic Ca2+ handling prior to heart failure might impact mitochondrial function during the compensatory phase of RV hypertrophy.
Does monocrotaline-induced pulmonary artery hypertension alter mitochondrial calcium fluxes and function in right ventricular cardiomyocytes in male Wistar rats?
Population
Male Wistar rats
Comparison
Monocrotaline injection vs saline injection
Design
Animal experimental study
Follow-up
Four weeks
Authors
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May indicate compensatory mitochondrial Ca2+ handling in rat RV hypertrophy; leaves open translation to human PAH.
Does monocrotaline-induced pulmonary artery hypertension alter mitochondrial calcium fluxes and function in right ventricular cardiomyocytes in male Wistar rats?
In a rat model of pulmonary artery hypertension, hypertrophic right ventricular cardiomyocytes exhibit larger mitochondrial calcium transients, likely as a compensatory mechanism to match ATP supply to increased energy demands.
Krstic et al. (2023) studied Pulmonary artery hypertension and right ventricular hypertrophy. Monocrotaline (MCT) vs. Saline (CON) was evaluated on Beat-to-beat mitochondrial Ca2+ fluxes, mitochondrial abundance and function. Monocrotaline-induced hypertrophic right ventricular cardiomyocytes had larger cytosolic and mitochondrial Ca2+ transients and increased mitochondrial protein abundance compared to saline controls.
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