Title: T-Tubule - an overview | ScienceDirect Topics
Headings: T-Tubule
T-Tubule
Ion Channel Trafficking
T-Tubules
Skeletal Muscle
T-tubules Are Surface Invaginations; the SR Is an Internal Membrane System
Structure and Function of Calcium Release Channels
2 T Tubules and CRUs Revert to More Primitive Forms Under Pathological Conditions
Muscles
Coupling Action Potentials to Contraction
The Cellular Basis of Cardiac Contractility
The SR Releases Stored Ca 2+ to Activate Contraction
Disorders of Muscle Excitability
Calcium couples muscle membrane excitation to filament contraction
Muscle physiology
Excitation–contraction coupling
EXERCISE | Muscle
Voltage-dependent Sarcoplasmic Reticulum Ca 2+ Release

Content: Cardiac muscle function is extremely dependent on well-regulated Ca 2+ movements, and thus it is highly sensitive to any alterations in the architecture of its SR/T tubule membrane system. Minor as well as profound alterations in Ca 2+ regulation and T tubule architecture have been detected in cardiac hypertrophy and failure ( Bers, 2006 ), reviewed by Brette and Orchard (2007). In view of these changes in the relationship between T tubules, CRUs and the myofibrils, several questions need to be addressed. One is whether changes in T tubule architecture are the cause of the result of the pathology; the second is whether T tubule disorder signals a disconnection of T tubules from CRUs or of CRUs from the myofibrils. Since CRU anchor T tubules to the myofibrils, both would result in T network disarrangement. Further, is the disorder due to a regression from a fully differentiated architecture to a more primitive one, or is the expression of an ongoing process of degeneration and regeneration, where the latter does not achieve a final result? A partial answer to some of these questions comes from the observation that reduced e–c coupling effectiveness in experimental cardiac hypertrophy may be interpreted as a reduction in functional coupling of CaV1.2 and RyR2 channels ( Gomez et al., 1997) and traced to an apparent disconnection between RyR and CaV1.2 clusters in the failing heart ( Song et al., 2006 ).