Remodeling of excitation-contraction coupling in the heart: Inhibition of sarcoplasmic reticulum Ca2+ leak as a novel therapeutic approach

被引:19
作者
Neef S. [1 ]
Maier L.S. [1 ]
机构
[1] Abt. Kardiologie and Pneumologie/Herzzentrum, Georg-August-Universität Göttingen, 37075 Göttingen
关键词
Sarcoplasmic Reticulum; Ryanodine Receptor; Calcium Release Channel; Cardiac Ryanodine Receptor; SERCA2a Protein;
D O I
10.1007/s11897-007-0020-7
中图分类号
学科分类号
摘要
In the heart, excitation-contraction coupling is the central mechanism by which electrical activation is translated into cardiac contraction. In heart failure, several proteins involved in this finely concerted regulation are changed with respect to expression, phosphorylation status, and function leading to remodeling of excitation-contraction coupling. The present review article summarizes well known alterations in heart failure and focuses on recent findings especially regarding altered sarcoplasmic reticulum Ca2+ release process due to two distinct kinases, namely protein kinase A and Ca 2+/calmodulin-dependent kinase II. Furthermore, it highlights the translation of those findings into possible novel therapeutic approaches. Copyright © 2007 by Current Medicine Group LLC.
引用
收藏
页码:11 / 17
页数:6
相关论文
共 50 条
[1]  
Cleland J.G., Swedberg K., Follath F., Et al., Study Group on Diagnosis of the Working Group on Heart Failure of the European Society of Cardiology: The EuroHeart Failure survey programme - a survey on the quality of care among patients with heart failure in Europe. Part 1: patient characteristics and diagnosis, Eur Heart J, 24, pp. 442-463, (2003)
[2]  
Packer M., Sudden unexpected death in patients with congestive heart failure: A second frontier, Circulation, 72, pp. 681-685, (1985)
[3]  
Yano M., Ikeda Y., Matsuzaki M., Altered intracellular Ca2+ handling in heart failure, J Clin Invest, 115, pp. 556-564, (2005)
[4]  
Hasenfuss G., Pieske B., Calcium cycling in congestive heart failure, J Moll Cell Cardiol, 34, pp. 951-969, (2002)
[5]  
Wehrens X.H., Lehnart S.E., Marks A.R., Intracellular calcium release and cardiac disease, Annu Rev Physiol, 67, pp. 69-98, (2005)
[6]  
Bers D.M., Cardiac excitation-contraction coupling, Nature, 415, pp. 198-205, (2002)
[7]  
Antos C.L., Frey N., Marx S.O., Et al., Dilated cardiomyopathy and sudden death resulting from constitutive activation of protein kinase a, Circ Res, 89, pp. 997-1004, (2001)
[8]  
Maier L.S., Zhang T., Chen L., Et al., Transgenic CaMKIIδC overexpression uniquely alters cardiac myocyte Ca2+ handling: Reduced SR Ca2+ load and activated SR Ca2+ release, Circ Res, 92, pp. 904-911, (2003)
[9]  
Maier L.S., Bers D.M., Calcium, calmodulin, and calcium-calmodulin kinase II: Heartbeat to heartbeat and beyond, J Mol Cell Cardiol, 34, pp. 919-939, (2002)
[10]  
Maier L.S., Ziolo M.T., Bossuyt J., Et al., Dynamic changes in free Ca-calmodulin levels in adult cardiac myocytes, J Mol Cell Cardiol, 41, pp. 451-458, (2006)