Why the study?
Does increased passive stiffness or altered Ca2+ handling drive diastolic dysfunction in pressure-overload induced left ventricular concentric hypertrophy in rats?
Population
Rats subjected to aortic banding (AB) to induce left ventricular concentric hypertrophy
Comparison
Aortic banding (AB) vs Sham-operated rats
Design
Preclinical
Follow-up
6 weeks after surgery
Authors
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Passive stiffness drives diastolic dysfunction in pressure-overload hypertrophy despite improved Ca2+ handling; leaves open whether targeting stiffness benefits HFpEF.
Does increased passive stiffness or altered Ca2+ handling drive diastolic dysfunction in pressure-overload induced left ventricular concentric hypertrophy in rats?
In pressure-overload hypertrophy, diastolic dysfunction is driven by increased passive stiffness from fibrosis and altered titin phosphorylation, rather than impaired cardiomyocyte calcium handling.
Røe et al. (2017) studied this question.
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