It is well-known that taurine (TAU) concentration in the excitable tissues,
such as the myocardium is exceptionally high (up to 30 mM). TAU accumulation in the
cardiomyocytes is a transporter-mediated process. Therefore, this amino acid should
play a critical role in cardiac tissue. Several studies revealed that a decrease in cardiac
TAU could lead to atrophic cardiomyopathy and impaired cardiac function. At
subcellular levels, the effects of TAU on mitochondria and energy metabolism are an
essential part of its function in the heart. Besides, it has been found that exogenous
TAU supplementation significantly enhanced cardiac mitochondrial function and ATP
levels. In the current chapter, the effects of TAU on cardiovascular diseases linked with
mitochondrial impairment are highlighted, and the role of TAU as a cardioprotective
agent is discussed. The data collected here could provide clues in managing a wide
range of cardiovascular complications connected with the energy crisis and
mitochondrial dysfunction.
Keywords: Arrhythmia, Cardiovascular diseases, Cardiomyopathy, Energy Crisis, Heart disease, Mitochondrial impairment.
