SERCA2a in Heart Failure: Role and Therapeutic Prospects |
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Authors: | Davide?Gianni Joachim?Chan Judith?K?Gwathmey Email author" target="_blank">Federica?del?MonteEmail author Roger?J?Hajjar |
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Institution: | (1) Cardiovascular Research Centre, Heart Failure Center, Massachusetts General Hospital, Boston, Massachusetts;(2) Imperial College, London, UK;(3) Gwathmey Inc, Cambridge, MA and Harvard Medical School, Boston, Massachusetts;(4) Cardiovascular Research Center, Massachusetts General Hospital, 149 13th Street Rm. 4217, Charlestown, Massachusetts, 02129 |
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Abstract: | Ca2+ is a key molecule controlling several cellular processes, from fertilization to cell death, in all cell types. In excitable
and contracting cells, such as cardiac myocytes, Ca2+ controls muscle contractility. The spatial and temporal segregation of Ca2+ concentrations are central to maintain its concentration gradients across the cells and the cellular compartments for proper
function. SERCA2a is a cornerstone molecule for maintaining a balanced concentration of Ca2+ during the cardiac cycle, since it controls the transport of Ca2+ to the sarcoplasmic reticulum (SR) during relaxation. Alterations of the activity of this pump have been widely investigated,
emphasizing its central role in the control of Ca2+ homeostasis and consequently in the pathogenesis of the contractile defect seen with heart failure. This review focuses on
the molecular characteristics of the pump, its role during the cardiac cycle and the prospects derived from the manipulation
of SERCA2a for heart failure treatment. |
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Keywords: | Heart failure SERCA gene therapy sarcoplasmic reticulum |
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