Taurine and cardiac disease: state of the art and perspectives

Abstract

Taurine is a nonessential amino acid that has received much attention. Two organs, the heart and the brain, are known to produce their own taurine, but in very limited quantities. It is for this reason that supplementation with this amino acid is necessary. Today, taurine is present in almost all energy drinks. A very vast literature reported beneficial effects of taurine in hepatic dysfunction, gastrointestinal injury, kidney diseases, diabetes, and cardiovascular diseases. Most of its effects were attributed to its modulation of Ca2+ homeostasis as well as to its antioxidant properties. In this review, we will focus on the current status of taurine modulation of the cardiovascular system and discuss future avenues for its use as a supplement therapy in a specific cardiovascular disease, namely hypertrophy, and heart failure.

The Anti-Inflammatory Effect of Taurine on Cardiovascular Disease

“…Taurine causes a direct effect on blood vessel function when administered to arteries in vitro [27]. When taurine was administered to thoracic aortae harvested from male Wistar rats, vasorelaxation was induced in a dose-dependent manner via the opening of an unspecified potassium channel [27], possibly the delayed outward K + channel current [1], as impaired vasorelaxation is one of the main factors leading to CVDs [28]. Therefore, taurine-induced vasorelaxation may elicit a beneficial role in the progression of CVD.…”

“…As such, it is not clear whether taurine directly inhibits AngII via AT1R, blocks the conversion of AngI into AngII, or simply influences the signaling cascade of AngII in cardiac hypertrophy. Bkaily et al have proposed that short-term taurine supplementation may stimulate Ca 2+ -dependent mechanisms, whereby taurine is co-transported with Na + on cardiomyocytes, subsequently leading to an increase of [Na + ]i and [taurine]i [1]. The increase in [Na + ]i could signal the Na + /Ca 2+ exchanger, resulting in elevated [Ca 2+ ]i [1].…”

“…Bkaily et al have proposed that short-term taurine supplementation may stimulate Ca 2+ -dependent mechanisms, whereby taurine is co-transported with Na + on cardiomyocytes, subsequently leading to an increase of [Na + ]i and [taurine]i [1]. The increase in [Na + ]i could signal the Na + /Ca 2+ exchanger, resulting in elevated [Ca 2+ ]i [1]. Although short-term taurine supplementation may be beneficial, as cardiomyocytes rely on [Ca 2+ ]i for contractility function [1], further studies are required to examine the mechanism of taurine's effect on AngII in cardiac hypertrophy.…”

“…The increase in [Na + ]i could signal the Na + /Ca 2+ exchanger, resulting in elevated [Ca 2+ ]i [1]. Although short-term taurine supplementation may be beneficial, as cardiomyocytes rely on [Ca 2+ ]i for contractility function [1], further studies are required to examine the mechanism of taurine's effect on AngII in cardiac hypertrophy.…”

“…Taurine (2-aminoethanesulphonic acid) is a sulfur-containing α-amino acid abundantly expressed in animal tissues (including the brain, retina, muscles, and organs throughout the body) [1]. Taurine is present in high amounts in: shellfish (scallops, mussels, clams), red meat, organ meats, chicken, turkey, eggs, and more recently, in energy drinks [1]. Taurine can also be synthesized endogenously from dietary intake of methionine to the homocysteine conversion pathway in humans [2].…”