title: The transverse-axial tubular system of cardiomyocytes.
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 Ca(2+) 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 Ca(2+)-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.
authors.affiliation: Division of Physiology, Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Ferrantini
authors.forename: C
authors.initials: C
authors.lastname: Crocini
authors.forename: R
authors.initials: R
authors.lastname: Coppini
authors.forename: F
authors.initials: F
authors.lastname: Vanzi
authors.forename: C
authors.initials: C
authors.lastname: Tesi
authors.forename: E
authors.initials: E
authors.lastname: Cerbai
authors.forename: C
authors.initials: C
authors.lastname: Poggesi
authors.forename: F S
authors.initials: FS
authors.lastname: Pavone
authors.forename: L
authors.initials: L
authors.lastname: Sacconi
mesh_terms: D000200:Action Potentials; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000473:pathology / Q000503:physiopathology; D020013:Calcium Signaling; D056966:Excitation Contraction Coupling; D006331:Heart Diseases / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D032383:Myocytes, Cardiac / Q000502:physiology* / Q000648:ultrastructure*; D012508:Sarcolemma / Q000502:physiology / Q000648:ultrastructure