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Table 1 Involvement and therapeutic potential of taurine in physio-pathological conditions and diseases of skeletal muscle

From: Taurine: the appeal of a safe amino acid for skeletal muscle disorders

Condition Change in Taurine content /TauT Pathogenetic mechanisms related to changes in taurine content General symptoms Taurine targets Therapeutic Potential of Taurine
Post-natal development Age-dependent increase in TauT expression and intracellular content Delayed development and delayed acquisition of specific phenotypic properties; metabolic dysfunction Specie-specific (due to different sensitivity to taurine deficiency) Mitochondria; ion channels; calcium homeostasis and calcium dependent gene expression Taurine supplementation in formula for pre-term born infants; to ensure a proper skeletal muscle phenotype differentiation
Aging Decrease in Taurine content; no information on TauT expression Metabolic distress; calcium dependent dysfunction; reduced regenerating ability; reduced activity of free-oxygen radicals scavengers Sarcopenia; atrophy, weakness and fatigue degeneration, altered excitation–contraction coupling, impaired performance Ion channels; Calcium homeostasis; oxidative stress and atrophy To counteract the decrease in taurine content and the consequent reduction in chloride channel function and the alteration in calcium ion homeostasis; to ameliorate performance and muscle strength
Ischemia and reperfusion injury Decrease due to a compensatory taurine efflux Insufficient vaso-dilation in relation to muscle work; metabolic distress; oxidative stress Hyperkaliemia, muscle dysfunction; ROS-induced inflammation and damage Metabolic-sensitive channels; mitochondria To counteract hyper-kaliemia by inhibiting KATP and KCa2+ channels; to prevent ischemia-induced taurine loss
Myotonic syndromes and periodic paralyses Unknown Primary inherited channelopathies due to loss-of function mutations of ClC-1 chloride channel or gain-of-function mutations of Nav1.4 sodium channel Hyperexcitability and impaired muscle relaxation ClC-1 chloride channel; Nav1.4 sodium channel To reduce membrane hyper-excitability through:
opening of chloride channel and increase in gCl mediated by both short and long term actions; modulation of generation and propagation of action potential, by blocking sodium channel with a local-anesthetic like mechanism
Disuse Slow-to-fast decrease in taurine content; no change in TauT expression Myofiber phenotype transition in postural muscle; atrophy Atrophy, change in metabolism, slow-to-fast transition; weakness Ion channel function and expression; calcium homeostasis To counteract disuse-induced taurine loss; to counteract myofiber transition; potential counteraction of atrophy
Duchenne muscular dystrophy and related myopathies Change in content related to pathology phase; possible reduction of TauT expression Alteration of calcium homeostasis; calcium-related degeneration; oxidative stress and inflammation Progressive muscle degeneration and weakness; muscle fiber loss and fibrosis; sarcolemmal instability; altered calcium homeostasis; inflammation and oxidative stress Chloride channel and voltage-insensitive calcium permeable channels (Leak/TRP-like); SERCA; mitochondria To ameliorate muscle performance; to counteract taurine loss and to modulate calcium availability for contraction; to counteract contraction-induced ischemia. To contrast degeneration-induced decrease in gCl; adjuvant therapy in combination with glucocorticoids
  1. The table summarizes the main role of taurine in various conditions of skeletal muscle, indicating evidences in relation to changes in tissue content and potential site of taurine action. Please refer to text for more detailed information and specific references.
  2. TauT taurine transport system, SERCA sarco/endoplasmatic reticulum calcium ATPasi, gCl macroscopic chloride conductance, TRP transient receptor potential channels, ROS reactive oxygen species, KATP ATP-dependent potassium channels, KCa calcium activated potassium channels.