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Mechanisms Underlying Development of Taurine-Deficient Cardiomyopathy

1
Department of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36688, USA
2
Faculty of Biotechnology, Fukui Prefectural University, Fukui 910-1195, Japan
3
Department of Pharmacy, School of Pharmacy, Hyogo University of Health Sciences, Kobe 650-8530, Japan
4
Department of Biochemistry and Molecular Medicine, The George Washington University, Washington, DC 20037, USA
*
Author to whom correspondence should be addressed.
Deceased: 20 September 2014.
Received: 6 July 2020 / Revised: 6 August 2020 / Accepted: 7 August 2020 / Published: 14 August 2020
(This article belongs to the Special Issue Nutrient Deficiency and Drug Induced Cardiac Injury and Dysfunction)
Taurine is a ubiquitous β-amino acid that plays an essential role in ensuring normal mitochondrial and myocardial function. In the mitochondria, taurine reacts with a tRNA forming a 5-taurinomethyluridine conjugate that primarily regulates the biosynthesis of the mitochondria encoded protein, ND6, which serves as a subunit of complex I of the respiratory chain. Impaired formation of the taurine conjugate reduces activity of complex I and plays a central role in the pathophysiology of the mitochondrial disease MELAS (myopathy, encephalopathy, lactic acidosis and stroke-like episodes). The restoration of mitochondrial levels of the taurine conjugate enhances electron flux through the respiratory chain, thereby preventing at least some of the symptoms of MELAS. Taurine therapy also diminishes the severity of congestive heart failure, an observation that led to its approval for the treatment of congestive heart failure in Japan. The review article discusses the role of defective calcium handling, reduced ATP generation, enhanced oxidative stress and apoptosis in the development of taurine-deficient cardiomyopathy. Some patients suffering from congestive heart failure are taurine-deficient, an observation supporting the hypothesis that low taurine levels contribute to the severity of heart failure. Thus, mishandling of taurine leads to mitochondrial dysfunction, which is involved in the development of both MELAS and congestive heart failure. View Full-Text
Keywords: 5-taurinomethyluridine-tRNALeu(UUR); mitochondria encoded protein ND6; complex I activity; lactate production; superoxide generation; mitochondrial permeability transition 5-taurinomethyluridine-tRNALeu(UUR); mitochondria encoded protein ND6; complex I activity; lactate production; superoxide generation; mitochondrial permeability transition
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MDPI and ACS Style

Schaffer, S.W.; Ito, T.; Azuma, J.; Jong, C.J.; Kramer, J.H. Mechanisms Underlying Development of Taurine-Deficient Cardiomyopathy. Hearts 2020, 1, 86-98. https://0-doi-org.brum.beds.ac.uk/10.3390/hearts1020010

AMA Style

Schaffer SW, Ito T, Azuma J, Jong CJ, Kramer JH. Mechanisms Underlying Development of Taurine-Deficient Cardiomyopathy. Hearts. 2020; 1(2):86-98. https://0-doi-org.brum.beds.ac.uk/10.3390/hearts1020010

Chicago/Turabian Style

Schaffer, Stephen W.; Ito, Takashi; Azuma, Junichi; Jong, Chian J.; Kramer, Jay H. 2020. "Mechanisms Underlying Development of Taurine-Deficient Cardiomyopathy" Hearts 1, no. 2: 86-98. https://0-doi-org.brum.beds.ac.uk/10.3390/hearts1020010

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