Why the study?
Does CHF1/Hey2 overexpression prevent pathological hypertrophy and apoptosis in response to pressure overload in mice?
Population
Wild-type and transgenic mice overexpressing CHF1/Hey2 in the myocardium, and cultured neonatal myocytes…
Comparison
Ascending aortic banding and exposure to… vs Wild-type mice and sham-operated controls.
Design
Preclinical
Follow-up
1 week
Authors
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Does not inform clinical practice; leaves open CHF1/Hey2 as a therapeutic target in human pressure-overload HF.
Does CHF1/Hey2 overexpression prevent pathological hypertrophy and apoptosis in response to pressure overload in mice?
CHF1/Hey2 promotes physiological over pathological hypertrophy in response to pressure overload by suppressing apoptosis and regulating transcriptional pathways, suggesting a potential target for heart failure drug discovery.
Yu et al. (2009) studied this question.
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