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Global proteomics and pathway analysis of pressure-overload-induced heart failure and its attenuation by mitochondrial-targeted peptides.

Authors
  • Dai, Dao-Fu
  • Hsieh, Edward J
  • Chen, Tony
  • Menendez, Lorena G
  • Basisty, Nathan B
  • Tsai, Lauren
  • Beyer, Richard P
  • Crispin, David A
  • Shulman, Nicholas J
  • Szeto, Hazel H
  • Tian, Rong
  • MacCoss, Michael J
  • Rabinovitch, Peter S
Type
Published Article
Journal
Circulation Heart Failure
Publisher
Ovid Technologies Wolters Kluwer -American Heart Association
Publication Date
Sep 01, 2013
Volume
6
Issue
5
Pages
1067–1076
Identifiers
DOI: 10.1161/CIRCHEARTFAILURE.113.000406
PMID: 23935006
Source
Medline
Keywords
License
Unknown

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.

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