Why the study?
Does genetic deletion of CaMKIIdelta prevent pathological cardiac hypertrophy and remodeling after pressure overload in mice?
Population
CaMKIIdelta-null mice
Design
Preclinical
Authors
Loading...
CaMKIIdelta inhibition merits further preclinical testing in pressure overload; animal data leave open clinical translation.
Does genetic deletion of CaMKIIdelta prevent pathological cardiac hypertrophy and remodeling after pressure overload in mice?
CaMKIIdelta functions as an important transducer of stress stimuli involved in pathological cardiac remodeling in vivo, identifying it as a potential therapeutic target for maintaining cardiac function during pressure overload.
Backs et al. (2009) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: