Population
CaMKIIδ/γ double-knockout mice, transgenic CaMKIIδC-overexpressing mice, wild-type mice, and human end-stage…
Comparison
CaMKII genetic manipulation and in vitro CaMKII… vs Wild-type mice and nonfailing human donor hearts
Design
Preclinical
Authors
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Hypothesis-generating for diastolic stiffness modulation in heart failure; human validation required before clinical consideration.
CaMKII phosphorylates titin at conserved sites to lower passive force, a mechanism that is deranged in heart failure and contributes to altered diastolic stress.
Hamdani et al. (2013) studied this question.
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