Why the study?
Does PKG activation reduce myocardial passive stiffness by phosphorylating titin in human and canine left ventricles?
Population
Human and canine left ventricles, skinned myofibers, isolated myofibrils, recombinant human I-band titin…
Comparison
Protein Kinase G in the presence of 8-pCPT-cGMP vs Dephosphorylated state or basal state
Design
Preclinical
Authors
Loading...
Supports PKG-titin pathway for diastolic stiffness; hypothesis-generating for heart failure therapies.
Does PKG activation reduce myocardial passive stiffness by phosphorylating titin in human and canine left ventricles?
PKG-dependent phosphorylation of the titin N2-Bus reduces myocardial passive stiffness, highlighting a potential therapeutic mechanism for improving diastolic function in heart failure.
Krüger et al. (2008) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: