Transverse tubule remodelling: a cellular pathology driven by both sides of the plasmalemma?

Transverse tubule remodelling: a cellular pathology driven by both sides of the plasmalemma? Transverse (t)-tubules are invaginations of the plasma membrane that form a complex network of ducts, 200–400 nm in diameter depending on the animal species, that penetrates deep within the cardiac myocyte, where they facilitate a fast and synchronous contraction across the entire cell volume. There is now a large body of evidence in animal models and humans demonstrating that pathological distortion of the t-tubule structure has a causative role in the loss of myocyte contractility that underpins many forms of heart failure. Investigations into the molecular mechanisms of pathological t-tubule remodelling to date have focused on proteins residing in the intracellular aspect of t-tubule membrane that form linkages between the membrane and myocyte cytoskeleton. In this review, we shed light on the mechanisms of t-tubule remodelling which are not limited to the intracellular side. Our recent data have demonstrated that collagen is an integral part of the t-tubule network and that it increases within the tubules in heart failure, suggesting that a fibrotic mechanism could drive cardiac junctional remodelling. We examine the evidence that the linkages between the extracellular matrix, t-tubule membrane and cellular cytoskeleton should be considered as a whole when investigating the mechanisms of t-tubule pathology in the failing heart. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Biophysical Reviews Springer Journals

Transverse tubule remodelling: a cellular pathology driven by both sides of the plasmalemma?

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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2017 by International Union for Pure and Applied Biophysics (IUPAB) and Springer-Verlag GmbH Germany
Subject
Life Sciences; Biochemistry, general; Biological and Medical Physics, Biophysics; Cell Biology; Membrane Biology; Biological Techniques; Nanotechnology
ISSN
1867-2450
eISSN
1867-2469
D.O.I.
10.1007/s12551-017-0273-7
Publisher site
See Article on Publisher Site

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