![]() The present review discusses the possibility of targeting cardioprotective signalling pathways and genes activated in the athlete's heart to treat or prevent heart failure. It is now clear that several signalling molecules play unique roles in the regulation of pathological and physiological cardiac hypertrophy. It has also been shown that both physiologic and pathologic cardiac hypertrophy may display distinct biochemical and molecular signaling pathways ( Iemitsu et al., 2001 Heineke and Molkentin, 2006 Bernardo et al., 2010 ). Physiological hypertrophy is characterized by normal organization of cardiac structure and normal or enhanced cardiac function, whereas pathological hypertrophy is commonly associated with upregulation of fetal genes, fibrosis, cardiac dysfunction and increased mortality. Intermittent pressure overload resulted in histological and cellular abnormalities with diastolic dysfunction and vascular rarefaction, suggesting that it was the nature of the stimulus and not its duration that was pathological. Physiological cardiac hypertrophy in response to exercise training differs in its structural and molecular profile to pathological hypertrophy associated with pressure or volume overload in disease. Physiological hypertrophy has normal or enhanced systolic function, and the structure and tissue of the heart structure are also normal, which can help in heart functioning (Maillet et al. Cardiac concentrations of IGF1 but not endothelin 1 or angiotensin II. Cardiac hypertrophy that occurs in athletes (physiological hypertrophy) is a notable exception. Whereas pathological cardiac hypertrophy is mediated by the neuro-endocrine hormones endothelin 1 and angiotensin II ( ). Most of them have only a single function, but an increasing number of proteins are being identified as multifunctional. ![]() ![]() Cardiac enlargement is a characteristic of most forms of heart failure. ![]() In general, cardiac hypertrophy (an increase in heart mass) is a poor prognostic sign. However, eccentric hypertrophy under pathological conditions (myocardial infarction or dilated cardiomyopathy) can lead to wall dilation with preferential. ![]()
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