The transverse-axial tubular system of cardiomyocytes
Authors: Ferrantini C., Crocini C., Coppini R., Vanzi F., Tesi C., Cerbai E., Poggesi C., Pavone FS., Sacconi L.
Autors Affiliation: Division of Physiology, Department of Clinical and experimental Medicine, University of Florence, Florence, Italy; Centre of Molecular Medicine (C.I.M.M.B.A.), University of Florence, Florence, Italy; European Laboratory for Non-Linear Spectroscopy (LeNS), University of Florence, Sesto Fiorentino, Italy; Division of Pharmacology, Department “NeuroFarBa”, University of Florence, Florence, Italy; Department of Biology, University of Florence, Florence, Italy; Department of Physics and Astronomy, University of Florence, Sesto Fiorentino, Italy; National Institute of Optics (INO), National Research Council (CNR), Florence, Italy
Abstract: A characteristic histological feature of striated muscle cells is the presence of deep invaginations of the plasma membrane (sarcolemma), most commonly referred to as T-tubules or the transverse-axial tubular system (TATS). TATS mediates the rapid spread of the electrical signal (action potential) to the cell core triggering Ca2+ release from the sarcoplasmic reticulum, ultimately inducing myofilament contraction (excitation-contraction coupling). T-tubules, first described in vertebrate skeletal muscle cells, have also been recognized for a long time in mammalian cardiac ventricular myocytes, with a structure and a function that in recent years have been shown to be far more complex and pivotal for cardiac function than initially thought. Renewed interest in T-tubule function stems from the loss and disorganization of T-tubules found in a number of pathological conditions including human heart failure (HF) and dilated and hypertrophic cardiomyopathies, as well as in animal models of HF, chronic ischemia and atrial fibrillation. Disease-related remodeling of the TATS leads to asynchronous and inhomogeneous Ca2+-release, due to the presence of orphan ryanodine receptors that have lost their coupling with the dihydropyridine receptors and are either not activated or activated with a delay. Here, we review the physiology of the TATS, focusing first on the relationship between function and structure, and then describing T-tubular remodeling and its reversal in disease settings and following effective therapeutic approaches.
Journal/Review: CELLULAR AND MOLECULAR LIFE SCIENCES
Volume: 70 (24) Pages from: 4695 to: 4710
More Information: The research leading to these results received funding from the European Union Seventh Framework Programme (FP7/2007-2013) under Grant Agreements 241577, 241526, 228334 and 284464. This work has been also supported by the Italian Ministry for Education, University and Research in the framework of the Flagship Project NANOMAX and by Telethon-Italy (GGP13162). This work has been carried out in the framework of the research activities of ICON foundation supported by \”Ente Cassa di Risparmio di Firenze\”. We thank Professor Giovanni Delfino for useful discussions.DOI: 10.1007/s00018-013-1410-5Citations: 30data from “WEB OF SCIENCE” (of Thomson Reuters) are update at: 2019-10-20References taken from IsiWeb of Knowledge: (subscribers only)Connecting to view paper tab on IsiWeb: Click hereConnecting to view citations from IsiWeb: Click here