Population
Freshly isolated cardiomyocytes and whole hearts from two mouse models with the metabolic syndrome
Comparison
Acute β-adrenergic stimulation vs Control hearts and cardiomyocytes
Design
Preclinical
Authors
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ROS overproduction may impair β-adrenergic responses in metabolic syndrome; leaves open whether antioxidant strategies improve contractility.
In mice with metabolic syndrome, cardiomyocytes adapt to chronic stress by decreasing mitochondrial ROS production in response to acute β-adrenergic stimulation, potentially preventing excessive ROS levels.
Llano‐Diez et al. (2016) studied this question.
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