Global Proteomics and Pathway Analysis of Pressure-Overload–Induced Heart Failure and Its Attenuation by Mitochondrial-Targeted Peptides

Abstract

This study elucidates the signaling pathways significantly changed in pressure-overload-induced heart failure. The global attenuation of TAC-induced proteomic alterations by the mitochondrial-targeted peptide SS31 suggests that perturbed mitochondrial function may be an upstream signal to many of the pathway alterations in TAC and supports the potential clinical application of mitochondrial-targeted peptide drugs for the treatment heart failure.