کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8475302 | 1550447 | 2013 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A functional role for transverse (t-) tubules in the atria
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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چکیده انگلیسی
Mammalian ventricular myocytes are characterised by the presence of an extensive transverse (t-) tubule network which is responsible for the synchronous rise of intracellular Ca2Â + concentration ([Ca2Â +]i) during systole. Disruption to the ventricular t-tubule network occurs in various cardiac pathologies and leads to heterogeneous changes of [Ca2Â +]i which are thought to contribute to the reduced contractility and increased susceptibility to arrhythmias of the diseased ventricle. Here we review evidence that, despite the long-held dogma of atrial cells having no or very few t-tubules, there is indeed an extensive and functionally significant t-tubule network present in atrial myocytes of large mammals including human. Moreover, the atrial t-tubule network is highly plastic in nature and undergoes far more extensive remodelling in heart disease than is the case in the ventricle with profound consequences for the resulting systolic Ca2Â + transient. In addition to considering the functional role of the t-tubule network in the healthy and diseased atria we also provide an overview of recent data concerning the putative factors controlling the formation of t-tubules and conclude by posing some important questions that currently remain to be addressed and whether or not targeting t-tubules offers potential novel therapeutic possibilities for heart disease. This article is part of a Special Issue entitled “Calcium Signaling in Heart”.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 58, May 2013, Pages 84-91
Journal: Journal of Molecular and Cellular Cardiology - Volume 58, May 2013, Pages 84-91
نویسندگان
Katharine M. Dibb, Jessica D. Clarke, David A. Eisner, Mark A. Richards, Andrew W. Trafford,