A Genetic Mouse Model of Cardiac Hypertrophy and Failure
Over a decade ago we examined the hypothesis that the heart reacts to stress or injury as an endocrine response organ. Specifically, we tested the hypothesis that increased systemic release of the neurohormones angiotensin II, epinephrine, and endothelin were the stimulus for cardiac hypertrophy.
To avoid confounding effects of these hormones and their receptors (which potently increase blood pressure), we used genetic techniques to autonomously activate their signaling pathways by overexpressing their common signal transducer, Gaq.
The Gq mouse develops spontaneous cardiac hypertrophy, and can be further induced to progress to heart failure via cardiac myocyte apoptosis. The Gq mouse is widely used for genetic “rescues” of heart failure, and for research into transcriptional events associated with reactive cardiac hypertrophy.