Key result
Hypertrophied cardiomyocytes demonstrated resistance to HNE-induced cell death, characterized by a 2-fold increase in glycolysis and increased oxidation of HNE to 4-hydroxynonenoic acid.
Why the study?
Does phenylephrine-induced hypertrophy alter the bioenergetic response and survival of neonatal rat cardiomyocytes exposed to electrophilic stress?
Population
Neonatal rat cardiomyocytes (NRCMs)
Comparison
Phenylephrine treatment to induce hypertrophy… vs Control NRCMs stressed with HNE
Design
Preclinical
Authors
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May reflect compensatory adaptation in early hypertrophy; leaves open translation to human cardiac remodeling.
Does phenylephrine-induced hypertrophy alter the bioenergetic response and survival of neonatal rat cardiomyocytes exposed to electrophilic stress?
Hypertrophied cardiomyocytes exhibit a protected phenotype against electrophilic stress through enhanced glycolysis and electrophile metabolism, suggesting a compensatory bioenergetic adaptation during early cardiac remodeling.
Sansbury et al. (2011) studied Cardiac hypertrophy and oxidative stress. Phenylephrine (PE)-induced hypertrophy and 4-hydroxynonenal (HNE) stress vs. Control neonatal rat cardiomyocytes was evaluated on Energetics, cell death, and electrophile metabolism. Hypertrophied cardiomyocytes demonstrated resistance to HNE-induced cell death, characterized by a 2-fold increase in glycolysis and increased oxidation of HNE to 4-hydroxynonenoic acid.
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