Parvalbumin Reduction in Relation to Possible Perturbations of CA²⁺ -Homeostasis in Muscular Dystrophy

Abstract

It has been suggested that muscle wasting in muscular dystrophy is causally related to a perturbation of Ca²⁺ -homeostasis in the muscle fiber (8,525–530) due to an increased permeability of the sarcolemmal membrane. An elevated sarcoplasmic Ca²⁺ concentration would result from an increased Ca²⁺ -influx and would thus lead to an activation of Ca²⁺ -dependent proteases. Ca²⁺ has also been shown to play an important role in the regulation of glucose-1,6-biphosphate (531,532) a powerful effector of several enzymes in glucose metabolism (533). This modulator has been shown to be significantly reduced in muscles of dystrophic mice (534,535).