期刊
CELL METABOLISM
卷 21, 期 2, 页码 183-194出版社
CELL PRESS
DOI: 10.1016/j.cmet.2015.01.005
关键词
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资金
- Cardiovascular Research Center at the Icahn School of Medicine at Mount Sinai Hospital
- National Institutes of Health
- American Heart Association
- Fondation Leducq
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.
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