Reversibility of T-tubule remodelling in heart failure: mechanical load as a dynamic regulator of the T-tubules.
The T-tubule system in ventricular cardiomyocytes is essential for synchronous Ca(2+) handling, and, therefore, efficient contraction. T-tubular remodelling is a common feature of heart disease. In this review, we discuss whether t-tubular remodelling can be reversed and which factors may be implicated in this process. In particular, we focus on the interaction between mechanical load variation and T-tubule structure and function. What is the evidence of this relationship? What is the role of different degrees and durations of mechanical load variation? In what settings might mechanical load variation have detrimental or beneficial effects on T-tubule structure and function? What are the molecular determinants of this interaction? Ultimately this discussion is used to address the question of whether mechanical load variation can provide an understanding to underpin attempts to induce recovery of the T-tubule system. In reviewing these questions, we define what remains to be discovered in understanding T-tubule recovery.
Laboratory of Cell Electrophysiology, 4th floor, Imperial Centre for Translational and Experimental Medicine, Hammersmith Campus, Du Cane Road, London W12 0NN, UK.
Michael
M
Ibrahim
Cesare M
CM
Terracciano
D000818:Animals; D002118:Calcium / Q000378:metabolism; D006333:Heart Failure / Q000473:pathology* / Q000503:physiopathology; D006353:Heart-Assist Devices; D006801:Humans; D008565:Membrane Proteins / Q000502:physiology; D032383:Myocytes, Cardiac / Q000473:pathology* / Q000502:physiology; D012519:Sarcoplasmic Reticulum / Q000473:pathology* / Q000502:physiology; D013314:Stress, Mechanical
D008565:Membrane Proteins; C412507:junctophilin; D002118:Calcium