Population
Single left ventricular myocytes from non-failing donor (n=6) and end-stage failing (n=10) human hearts
Comparison
Analysis of isoform composition and… vs Myocytes from non-failing donor hearts
Design
Preclinical
Authors
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Hypothesis-generating in animal HF models; leaves open translation to human disease mechanisms or therapies.
Increased Ca2+-responsiveness in end-stage failing human hearts is driven by changes in the phosphorylation status of MLC-2 and TnI rather than a shift in contractile protein isoforms.
Papp et al. (2002) studied this question.
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