September 1, 2000Journal of Biological ChemistryOpen Access

ε Protein Kinase C in Pathological Myocardial Hypertrophy

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Population

Mouse hearts with Galpha(q) overexpression (a PKC-linked hypertrophy signal transducer)

Comparison

Co-expression of epsilonPKC-selective… vs Galpha(q) overexpression alone

Design

Preclinical

Authors

GWGuangyu WuZhejiang University TTTsuyoshi ToyokawaCincinnati Children's Hospital Medical Center HHHarvey HahnUniversity of Wisconsin–Madison

Discussion

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Implication

Supports compensatory epsilonPKC role in hypertrophy; hypothesis-generating and should not yet inform clinical practice.

Structured PICO

Population

Mouse hearts with Galpha(q) overexpression (a PKC-linked hypertrophy signal transducer)

Intervention

Co-expression of epsilonPKC-selective translocation inhibitor (epsilonV1) or activator (psiepsilonRACK) peptides

Comparator

Galpha(q) overexpression alone

Outcome

Cardiac contractile function measured as left ventricular fractional shortening and epsilonPKC particulate partitioningsurrogate

epsilonPKC signaling acts as a compensatory rather than pathological event in myocardial hypertrophy, suggesting therapeutic potential for selective epsilonPKC translocation enhancement in cardiac insufficiency.

Cite This Study

Wu et al. (2000) studied this question.

synapsesocial.com/papers/6a7c7e6bf78cd83d7f8f1388 https://doi.org/10.1074/jbc.c000380200

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ε Protein Kinase C in Pathological Myocardial Hypertrophy

Discussion

Member takes

Implication

Structured PICO

Cite This Study

ε Protein Kinase C in Pathological Myocardial Hypertrophy

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider