Key result
Acute myocardial stretching reduces EDP ~40% via cGMP-PKG-mediated titin phosphorylation.
Why the study?
Does acute stretching induce adaptive changes in myocardial compliance in experimental models and humans?
Does acute stretching induce adaptive changes in myocardial compliance in experimental models and humans?
Effect estimate: >40% decrease
Acute cardiac stretching induces a novel adaptive increase in myocardial compliance mediated by titin phosphorylation via cGMP-PKG signaling, which is impaired in left ventricular hypertrophy.
No takes yet. Share an insight, caveat, or question.
Should not yet change practice in diastolic dysfunction; leaves open titin-PKG modulation as a target in human hypertrophy.
Leite-Moreira et al. (2018) studied Acute cardiac load. Acute stretching / volume loading vs. Non-stretched myocardium / baseline was evaluated on End-diastolic pressure (EDP) or passive tension (PT) (>40% decrease). Acute myocardial stretching induced a sustained >40% decrease in end-diastolic pressure or passive tension, mediated by titin phosphorylation through cGMP-PKG signalling.
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