Metabolic Remodelling of the Hypertrophied Heart

Abstract

The heart develops hypertrophy in response to persistent elevation in cardiac workload. Depending on the nature of the stimulus, cardiac hypertrophy can be categorized as pathologic or physiologic, each of which is accompanied by distinctly different phenotypic alterations including alterations in energy metabolism. These unique metabolic phenotypes may, in part, explain the differing functional outcomes of pathologically and physiologically hyper-trophied hearts, especially notable following an ischemic stress. Thus, the mechanisms underlying remodelling in pathologic and physiologic cardiac hypertrophy have been the focus of many studies. A number of molecules including AMP-activated protein kinase, peroxisome proliferator-activated receptor-a, peroxisome proliferator-activated receptor gamma coactivator 1, protein kinase C, phosphoinositide-3 kinase/protein kinase B, and reac-tive oxygen species have been implicated as participating in the process of metabolic remodelling in cardiac hypertrophy.