Does the loss of transverse tubules contribute to dyssynchronous Ca 2+ release during heart failure?

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See article by Louch et al. [1] (pages 63–73) in this issue. Congestive heart failure (CHF) is the leading cause of death in developed countries. This syndrome is due to the incapacity of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues. Very often CHF is caused by a defect in myocardial contraction. Thereby, a better understanding of the cellular and molecular basis of the altered contractility of failing heart is a major research topic of many laboratories in the hopes of identifying new targets for the treatment of CHF. The manuscript of Louch et al. [1] in the current issue of Cardiovascular Research examines the possibility that alteration of the microarchitecture of cardiac myocytes, specifically of the transverse (T) tubule system, plays a role in the defective excitation–contraction coupling (EC coupling) process of ventricular myocytes from human failing hearts. In mammalian cardiac myocytes, contraction is controlled by a sequence of events that includes the activation of the L-type Ca2+ current, which in turn triggers the opening of the Ca2+ release channels [ryanodine receptors of the sarcoplasmic reticulum (SR), RyRs] and the release of Ca2+ from the sarcoplasmic reticulum in keeping with the Ca2+-induced Ca2+ release phenomenon (CICR). The close proximity of the RyRs and the L-type Ca2+ channels in dyadic junctions of the T-tubules provides for privileged Ca2+ cross-signaling between the … *Tel.: +33-1-40-25-86-00; fax: +33-1-40-25-86-02. Email address: hatem{at}




Hatem, S. (2004, April 1). Does the loss of transverse tubules contribute to dyssynchronous Ca 2+ release during heart failure? Cardiovascular Research, 62(1), 1–3.

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