A Role of Endogenous Taurine in Mitochondrial Metabolism in Mice Primary Skeletal Muscle

Abstract

Muscular dystrophy and neuromuscular diseases have been persisting and its causes range from genetic inheritance to injuries, resulting in muscle weakening and paralysis. In consideration of muscle contraction and its relevance to the mitochondria, an investigation into primary skeletal muscle cells was carried out to observe the amino acid taurine, focusing on its effect on the mitochondria from a cellular level. It was concluded that taurine may slow down the progressive muscle weakness and aging through enhancing calcium homeostasis and suppressing the production of ROS. Taurine deficiency could also be associated with aging animals, indicating that taurine may have anti-aging actions. Thus, it was assumed that taurine deficiency is associated with the increase in aging-associated tissue damage, reducing the life span of the mouse model by knocking out the taurine transporter. In addition, it was concluded that a reduce in taurine level is associated with the rise of unfolded protein response (UPR), meaning that the protein folding by taurine can be improved.