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- Title
The transverse-axial tubular system of cardiomyocytes.
- Authors
Ferrantini, C.; Crocini, C.; Coppini, R.; Vanzi, F.; Tesi, C.; Cerbai, E.; Poggesi, C.; Pavone, F. S.; Sacconi, L.
- 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.
- Subjects
HEART cells; STRIATED muscle; MUSCLE cells; CELL membranes; SARCOPLASMIC reticulum; CYTOPLASMIC filaments; HEART failure
- Publication
Cellular & Molecular Life Sciences, 2013, Vol 70, Issue 24, p4695
- ISSN
1420-682X
- Publication type
Article
- DOI
10.1007/s00018-013-1410-5