Abstract

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.