![]() In this Review, we summarize the underlying molecular mechanisms of physiological and pathological hypertrophy, with a particular emphasis on the role of metabolic remodelling in both forms of cardiac hypertrophy, and we discuss how the current knowledge on cardiac hypertrophy can be applied to develop novel therapeutic strategies to prevent or reverse pathological hypertrophy. In the past decade, a growing number of studies have suggested that previously unrecognized mechanisms, including cellular metabolism, proliferation, non-coding RNAs, immune responses, translational regulation, and epigenetic modifications, positively or negatively regulate cardiac hypertrophy. no fibrosis or apoptosis) and normal or enhanced cardiac function. the 'athlete's heart') is reversible and is characterized by normal cardiac morphology (i.e. ![]() Each form of hypertrophy is regulated by distinct cellular signalling pathways. In contrast, physiological cardiac hypertrophy (heart growth that occurs in response to chronic exercise training, i.e. Hypertrophy initially develops as an adaptive response to physiological and pathological stimuli, but pathological hypertrophy generally progresses to heart failure. There are two types of hypertrophy: physiological and pathological. Therefore, in the adult heart, instead of an increase in cardiomyocyte number, individual cardiomyocytes increase in size, and the heart develops hypertrophy to reduce ventricular wall stress and maintain function and efficiency in response to an increased workload. ‘Pathological’ cardiac hypertrophy is a condition that is characterized by the thickening of the heart muscle, a decrease in the size of the chambers of the heart, and a reduced capacity of the heart to pump blood to the tissues and organs around the body. Cardiomyocytes exit the cell cycle and become terminally differentiated soon after birth.
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