Heart failure (HF) is a common disease that has been attributed, in part, to deprivation of cardiac energy. As a result, the interplay between metabolism and adenosine triphosphate production is fundamental in determining the mechanisms driving the disease progression. Due to its central role in energy production, metabolism, calcium homeostasis, and oxidative stress, the mitochondrion has been suggested to play a pivotal role in the progression of the heart to failure. Nevertheless, the mitochondrion's specific role(s) and the proteins contributing to the development and progression of HF are not entirely clear. Thus, changes in mitochondrial proteomic make-up during HF have garnered great interest. With the continued development of advanced tools for assessing proteomic make-up, characterization of mitochondrial proteomic changes during disease states such as HF are being realized. These studies have begun to identify potential biomarkers of disease progression as well as protein targets that may provide an avenue for therapeutic intervention. The goal of this review is to highlight some of the changes in mitochondrial proteomic make-up that are associated with the development of HF in an effort to identify target axes and candidate proteins contributing to disease development. Results from a number of different HF models will be evaluated to gain insight into some of the similarities and differences in mitochondrial proteomic alterations associated with morphological and functional changes that result from the disease. Congest Heart Fail.
© 2011 Wiley Periodicals, Inc.