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 |