Intracellular devastation in heart failure.
End-stage heart failure is characterized by a number of abnormalities at the cellular level, which include changes in excitation-contraction coupling, alterations in contractile proteins and activation/deactivation of signaling pathways. Even though many of these changes are adaptive to the high workload and stress in heart failure, a significant number of these alterations are deeply deleterious to the cardiac cell. In this article, we will review the changes in calcium cycling that occur in myopathic hearts and how they can be effectively targeted. We will also focus on protein misfolding in the setting of cardiac dysfunction.
Del Monte
Federica
F
Cardiovascular Research, Beth Israel Deaconess Medical Center, 330 Brookline Ave., Boston, MA 02215, USA. fdelmont@bidmc.harvard.edu
Hajjar
Roger J
RJ
D000818:Animals; D017209:Apoptosis; D002118:Calcium / Q000378:metabolism*; D004721:Endoplasmic Reticulum / Q000378:metabolism; D006333:Heart Failure / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D008565:Membrane Proteins / Q000378:metabolism; D009200:Myocardial Contraction / Q000502:physiology; D032383:Myocytes, Cardiac / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology
D008565:Membrane Proteins; D002118:Calcium