Why the study?
How do hypertension and exercise differentially affect cardiac proteome remodeling and hypertrophy?
How do hypertension and exercise differentially affect cardiac proteome remodeling and hypertrophy?
Exercise induces cardioprotective proteomic changes that lead to physiologic cardiac hypertrophy, which differs fundamentally from the pathologic proteome remodeling caused by hypertension.
Supports distinct proteomic signatures in physiologic versus pathologic hypertrophy; leaves open clinical translation or targeted interventions.
Left ventricle hypertrophy is a common outcome of pressure overload stimulus closely associated with hypertension. This process is triggered by adverse molecular signalling, gene expression, and proteome alteration. Proteomic research has revealed that several molecular targets are associated with pathologic cardiac hypertrophy, including angiotensin II, endothelin-1 and isoproterenol. Several metabolic, contractile, and stress-related proteins are shown to be altered in cardiac hypertrophy derived by hypertension. On the other hand, exercise is a nonpharmacologic agent used for hypertension treatment, where cardiac hypertrophy induced by exercise training is characterized by improvement in cardiac function and resistance against ischemic insult. Despite the scarcity of proteomic research performed with exercise, healthy and pathologic heart proteomes are shown to be modulated in a completely different way. Hence, the altered proteome induced by exercise is mostly associated with cardioprotective aspects such as contractile and metabolic improvement and physiologic cardiac hypertrophy. The present review, therefore, describes relevant studies involving the molecular characteristics and alterations from hypertensive-induced and exercise-induced hypertrophy, as well as the main proteomic research performed in this field. Furthermore, proteomic research into the effect of hypertension on other target-demerged organs is examined.
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Petriz et al. (2014) studied this question.
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