Reexpression of T-type Ca channels after myocardial infarction: does it play a role in cardiac excitation?

Abstract

See article by Huang et al. [5] (pages 442–449) in this issue. Electrophysiological and myocardial remodeling plays an important role in the development of heart failure and arrhythmogenesis after myocardial infarction. Previous reports [1–4] have shown that the activation of signal transduction pathways after myocardial infarction involved in the initiation of cardiac hypertrophy follows a distinct pattern. Why do fetal and neonatal isogenes become reactivated under pathologic conditions? Recent studies [5–7] have taught us that expression and function of ion channels is very dynamic and can be affected at various levels depending on various physiologic and adverse stimuli. The pattern of cardiac excitation, pathologic stimuli such as ischemia or infarction and rate of impulse propagation have important effects on ion channel expression and properties. The number, biophysical characteristics and distribution of ion channels is affected by mRNA transcription and protein translation rates, post-translational modifications, rate of cellular turn-over of ion channel proteins and phosphorylation level of important amino acid residues on the channel protein. Huang and his associates [5] present data that is of substantial importance in enhancing our understanding of the underlying mechanisms of ionic remodeling after myocardial infarction. Specifically, they present data on the reexpression of T-type Ca channel in post-infarction viable left ventricular myocytes. In the heart, two types of Ca channels have been identified that are expressed on the sarcolemma of cardiomyocytes: the longlasting type of high voltage activated Ca channel ( I Ca, L) and the low voltage activated transient Ca channel ( I Ca, T). The L-type Ca current plays an important role in maintaining the plateau phase of the action potential, … * Tel.: +31-30-2566-566; fax: +31-30-2566-738