Abstract

The heart experiences constantly changing demands that require morphological and functional alterations to maintain adequate cardiovascular perfusion. Upon exposure to pathological stimuli, the heart responds by dramatically inducing biochemical signaling and gene expression that alter cardiomyocyte cell size, maximize or change the source of energy substrates, and increase cardiac output. Cardiac remodeling, whether through anabolic or catabolic processes, initially improves or maintains cardiac function. However, with sustained cardiac stress, cellular processes mediating cell survival, metabolism, and the maintenance of normal cardiac architecture begin to fail.

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