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Another active area of research in the laboratory focuses on unraveling the mechanisms behind maladaptive, or pathological, and adaptive, or physiological, cardiac hypertrophy. In response to certain stresses, such as exercise and pregnancy, physiological cardiac hypertrophy can develop but is often fully reversible upon removal of the stimuli. In contrast, pathological hypertrophy, often a result of hypertension, aortic valve stenosis, or chronic adrenergic receptor stimulation, is considered irreversible even when the pathological stimulus is removed or corrected. Both forms of cardiac hypertrophy differ in their structural and molecular profiles.
To uncover the mechanisms involved in both the development of cardiac hypertrophy, and the regression from this hypertrophic state, the laboratory uses several different model systems including the Burmese python. The Burmese python undergoes significant cardiac hypertrophy following consumption of a large meal. Within 10-15 days, the adaptive cardiac hypertrophy within the Burmese python fully regresses and is no longer significantly bigger compared to fasted controls. Thus, along with pregnancy and exercise models, we use the Burmese python as a model of physiological hypertrophy.
To contrast our models of physiological hypertrophy, we employ several different models of pathological hypertrophy. These include acute or chronic adrenergic stimulation, high-fat (or Western) diets, pressure overload, and myocardial infarction models. Using both physiological and pathological model systems, we are able to compare and contrast the pathology underscoring both classifications of cardiac hypertrophy.