Altered Ca2+ sparks in aging skeletal and cardiac muscle.
Ca2+ sparks are the fundamental units that comprise Ca2+-induced Ca2+ release (CICR) in striated muscle cells. In cardiac muscle, spontaneous Ca2+ sparks underlie the rhythmic CICR activity during heart contraction. In skeletal muscle, Ca2+ sparks remain quiescent during the resting state and are activated in a plastic fashion to accommodate various levels of stress. With aging, the plastic Ca2+ spark signal becomes static in skeletal muscle, whereas loss of CICR control leads to leaky Ca2+ spark activity in aged cardiomyocytes. Ca2+ spark responses reflect the integrated function of the intracellular Ca2+ regulatory machinery centered around the triad or dyad junctional complexes of striated muscles, which harbor the principal molecular players of excitation-contraction coupling. This review highlights the contribution of age-related modification of the Ca2+ release machinery and the effect of membrane structure and membrane cross-talk on the altered Ca2+ spark signaling during aging of striated muscles.
Weisleder
Noah
N
Department of Physiology and Biophysics, Robert Wood Johnson Medical School, 675 Hoes Lane, Piscataway, NJ 08854, USA.
Ma
Jianjie
J
D000375:Aging / Q000378:metabolism*; D000818:Animals; D020013:Calcium Signaling; D006801:Humans; D007425:Intracellular Membranes / Q000648:ultrastructure; D051379:Mice; D009124:Muscle Proteins / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000648:ultrastructure; D009206:Myocardium / Q000378:metabolism*; D020239:Receptor Cross-Talk; D016708:Synaptophysin / Q000378:metabolism
C111842:Mg29 protein, mouse; D009124:Muscle Proteins; D016708:Synaptophysin