Cytoskeletal basis of ion channel function in cardiac muscle.

The heart is a force-generating organ that responds to self-generated electrical stimuli from specialized cardiomyocytes. This function is modulated by sympathetic and parasympathetic activity. In order to contract and accommodate the repetitive morphological changes induced by the cardiac cycle, cardiomyocytes depend on their highly evolved and specialized cytoskeletal apparatus. Defects in components of the cytoskeleton affect the ability of the cell to compensate at both functional and structural levels in the long term. In addition to structural remodeling, the myocardium becomes increasingly susceptible to altered electrical activity, leading to arrhythmogenesis. The development of arrhythmias secondary to structural remodeling defects has been noted, although the detailed molecular mechanisms are still elusive. Here, the author reviews the current knowledge of the molecular and functional relationships between the cytoskeleton and ion channels, and discusses the future impact of new data on molecular cardiology research and clinical practice.