Key result
p90RSK acts downstream of PKCbetaII and mediates redox-sensitive cardiac troponin I phosphorylation in cardiomyocytes, which was prevented by p90RSK inhibition or the PKCbeta inhibitor LY333,531.
Population
Mice models and in vitro cardiomyocyte models
Comparison
Genetic manipulation and pharmacological… vs Wild type mice and untreated controls
Design
Preclinical
Authors
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p90RSK-PKCbetaII signaling may modulate redox cTnI effects in cardiomyocytes; hypothesis-generating for heart failure therapies pending human validation.
The study identifies p90RSK as a downstream effector of PKCbeta II that mediates redox-sensitive cTnI phosphorylation in cardiomyocytes, revealing a novel mechanism potentially involved in heart failure progression.
Itoh et al. (2005) studied Heart failure / Cardiac troponin I phosphorylation. p90RSK modulation and LY333,531 vs. Wild type / Control was evaluated on cTnI (Ser23/24) phosphorylation. p90RSK acts downstream of PKCbetaII and mediates redox-sensitive cardiac troponin I phosphorylation in cardiomyocytes, which was prevented by p90RSK inhibition or the PKCbeta inhibitor LY333,531.
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