Effect of taurine on ischemia–reperfusion injury

• Published in: Amino acids 2014-01, Vol.46 (1), p.21-30
• Main Authors: Schaffer, Stephen W, Jong, Chian Ju, Ito, Takashi, Azuma, Junichi
• Format: Article
• Language: English
• Subjects: Activation; Analytical Chemistry; Animals; Biochemical Engineering; Biochemistry; Biomedical and Life Sciences; Calcium - metabolism; Cell Death; electron transport chain; extrusion; heart; heart failure; Heart Failure - etiology; Heart Failure - metabolism; Heart Failure - pathology; heart transplant; Humans; Life Sciences; myocardial infarction; Myocardial Reperfusion Injury - complications; Myocardial Reperfusion Injury - metabolism; Myocardial Reperfusion Injury - pathology; Neurobiology; permeability; Proteomics; reactive oxygen species; Reactive Oxygen Species - metabolism; Review Article; risk; Signal Transduction; Sodium - metabolism; taurine; Taurine - metabolism; Ventricular Remodeling
• ISSN: 0939-4451; 1438-2199
• DOI: 10.1007/s00726-012-1378-8

Taurine is an abundant β-amino acid that regulates several events that dramatically influence the development of ischemia–reperfusion injury. One of these events is the extrusion of taurine and Na⁺from the cell via the taurine/Na⁺symport. The loss of Na⁺during the ischemia–reperfusion insult limits the amount of available Na⁺for Na⁺/Ca²⁺exchange, an important process in the development of Ca²⁺overload and the activation of the mitochondrial permeability transition, a key process in ischemia–reperfusion mediated cell death. Taurine also prevents excessive generation of reactive oxygen species by the respiratory chain, an event that also limits the activation of the MPT. Because taurine is an osmoregulator, changes in taurine concentration trigger “osmotic preconditioning,” a process that activates an Akt-dependent cytoprotective signaling pathway that inhibits MPT pore formation. These effects of taurine have clinical implications, as experimental evidence reveals potential promise of taurine therapy in preventing cardiac damage during bypass surgery, heart transplantation and myocardial infarction. Moreover, severe loss of taurine from the heart during an ischemia–reperfusion insult may increase the risk of ventricular remodeling and development of heart failure.