Does the loss of transverse tubules contribute to dyssynchronous Ca2+ release during heart failure?

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