Key result
CHOP deficiency attenuates pressure overload-induced cardiac hypertrophy, fibrosis, and dysfunction.
Why the study?
The role of endoplasmic reticulum-initiated apoptotic signaling in the development of heart failure was not well clarified.
Does CHOP deficiency prevent cardiac hypertrophy and dysfunction induced by pressure overload in mice?
Population
Myocardial samples from patients with heart failure and wild-type and CHOP-deficient mice
Comparison
CHOP-deficient mice vs wild-type mice after transverse aortic constriction
Design
Experimental study with transverse aortic constriction and sham operation in mice
Follow-up
4 weeks
Authors
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Suggests ER stress contributes to human HF; hypothesis-generating for CHOP-targeted therapies.
Does CHOP deficiency prevent cardiac hypertrophy and dysfunction induced by pressure overload in mice?
Genetic ablation of CHOP attenuates endoplasmic reticulum-mediated apoptosis and cardiac dysfunction in a mouse model of pressure overload, highlighting a potential novel mechanism in heart failure development.
Fu et al. (2010) studied Heart failure and cardiac hypertrophy. CHOP deficiency vs. Wild-type (WT) was evaluated on Cardiac hypertrophy, fibrosis, and cardiac dysfunction. CHOP deficiency attenuated cardiac hypertrophy, fibrosis, and dysfunction at 4 weeks after transverse aortic constriction compared with wild-type mice.
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