Short-Communication: Short-Term Treatment with Taurine Prevents the Development of Cardiac Hypertrophy and Early Death in Hereditary Cardiomyopathy of the Hamster and Is Sex-Dependent

Abstract

Premature death due to heart failure is a major health problem. Taurine is a non-essential amino acid that has received much attention. However, although many studies have been carried out on the beneficial effects of taurine in cardiac pathophysiology, no studies have investigated the effect of taurine treatment on the development of hereditary cardiomyopathy (HCM) associated with hypertrophy, heart failure, and early death. This study aims to verify whether short-term treatment (20 days) with taurine in tap water prevents the development of hypertrophy and premature death in hereditary cardiomyopathy of the hamster (HCMH) of the line UM-X7.1 and if its effect is sex-dependent. Our results show that treatment for 20 days with taurine (250 mg/kg/day or 25 mg/animal/day) during the development of the hypertrophic phase (220 days old) significantly decreased (p < 0.01) the heart weight to body weight ratio in male HCMHs without affecting the female. During the 20 days (220–240 days old), there were nearly 40% premature deaths in non-treated males HCMHs and 50% in female HCMHs. Treatment for 20 days wholly and significantly prevented early death in both males and females HCMHs. Our results demonstrate that short-term treatment with taurine prevents the development of cardiac hypertrophy associated with HCM in a sex-dependent manner; however, it prevents early death in a sex-independent fashion. Our results suggest that taurine supplementation could be used to treat HCM.

Taurine Prevents Angiotensin II-Induced Human Endocardial Endothelium Morphological Remodeling and the Increase in Cytosolic and Nuclear Calcium and ROS

“…This should be verified in the future. In addition, the prevention of Ang II-induced hypertrophy and increase in intracellular free calcium could be due to the long-term effect of taurine in reducing calcium overload [ 18 , 19 ]. Our results also show that taurine prevents Ang II-induced increase in cytosolic ROS without affecting the increase in ROS at the nucleoplasmic level.…”

“…In conclusion, our results clearly show that Ang II does induce hypertrophy of EECs, and these types of cells may contribute to the overall effect of Ang II in the heart. In addition, taurine’s prevention of Ang II-induced EEC hypertrophy demonstrates that the preventive effect of this nonessential amino acid on cardiac hypertrophy in hereditary cardiomyopathy [ 18 , 19 ] is due, at least in part, to its prevention of EEC hypertrophy.…”

“…The increase in intracellular ROS by Ang II was reported to be mediated via the activation of c-Src causing an increase in NOX activity [ 17 ] and, more particularly, the Ca 2+ -dependent NOX5. In addition, taurine, a nonessential amino acid, is a well-known endogenous antioxidant and was recently reported to prevent the development of hypertrophy associated with heart failure and early death [ 18 , 19 ]. However, verifying whether taurine prevents Ang II’s effect on EECs via reducing Ang II-induced cell hypertrophy associated with increased intracellular ROS awaits verification.…”

Short Communication: Taurine Long-Term Treatment Prevents the Development of Cardiac Hypertrophy, and Premature Death in Hereditary Cardiomyopathy of the Hamster Is Sex-Independent

“…This powerful antioxidant has been reported to block and prevent many pathologies related to the neural, renal, and cardiovascular systems [14,16,17]. Recently, using the UMX-7.1 cardiomyopathic hamster animal model, our group demonstrated that short-term taurine supplementation prevents the development of hypertrophy in males but not in females [18].…”

“…Furthermore, the degree of severity of hypertrophy and heart failure is higher in females than in males [18]. For these reasons, it is possible to postulate that the difference in the effect of short-term taurine treatment between males and females in hereditary cardiomyopathy is due to the extent of damage, which is more significant in females than in males, and the fact that long-term treatment may generate a sex-independent effect.…”