Altered myocardial calcium cycling and energetics in heart failure--a rational approach for disease treatment

Cell Metab. 2015 Feb 3;21(2):183-194. doi: 10.1016/j.cmet.2015.01.005.


Cardiomyocyte function depends on coordinated movements of calcium into and out of the cell and the proper delivery of ATP to energy-utilizing enzymes. Defects in calcium-handling proteins and abnormal energy metabolism are features of heart failure. Recent discoveries have led to gene-based therapies targeting calcium-transporting or -binding proteins, such as the cardiac sarco(endo)plasmic reticulum calcium ATPase (SERCA2a), leading to improvements in calcium homeostasis and excitation-contraction coupling. Here we review impaired calcium cycling and energetics in heart failure, assessing their roles from both a mutually exclusive and interdependent viewpoint, and discuss therapies that may improve the failing myocardium.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Calcium-Transporting ATPases / metabolism
  • Heart Failure / metabolism*
  • Humans
  • Myocardium / metabolism*


  • Calcium-Transporting ATPases
  • Calcium