Taurine is a semiessential amino acid found at high concentrations in mammalian plasma and cells, where it regulates cellular functions such as ion flux, controls cell volume and serves as a substrate for conjugated bile acids (BAs). Exogenous administration of both taurine and taurine-conjugated BAs have also been implicated in the modulation of cardiovascular functions. This brief review summarizes the role of taurine and taurine-conjugated BAs in vascular relaxation through the modulation of endothelium-derived nitric oxide (NO). The effects of taurine on vascular health are controversial. However, in the presence of cardiometabolic risk factors, it has been proposed that taurine can increase vascular NO levels by increasing eNOS expression, eNOS phosphorylation on Ser1177, NO bioavailability, the level of antioxidative defense, and the l-arginine/NOS inhibitor asymmetric dimethylarginine (ADMA) ratio. The taurine-conjugated BA-mediated activation of Farnesoid X receptor (FXR), G protein-coupled BA receptor (TGR5) and/or muscarinic 3 receptor (M3) was also reported to increase vascular NO production. FXR activation increases eNOS expression and may reduce ADMA formation, while TGR5 increases mobilization of Ca2+ and phosphorylation of eNOS and Akt in endothelial cells. Furthermore, taurine and taurine-conjugated BAs might regulate NO synthesis and activity by enhancing H2S generation. Several studies have demonstrated the beneficial effects of both taurine and taurine-conjugated BAs in reversing the endothelial dysfunction associated with diabetes, atherosclerosis, hypertension, obesity, malnutrition, and smoking. In addition, taurine-conjugated BAs have emerged as a potential treatment for portal hypertension. Despite these favorable findings, there is a need to further explore the mechanisms and signaling pathways underlying the endothelial effects of taurine and taurine-conjugated BAs. Here, we summarize the main findings regarding the effects of taurine and taurine-conjugated BAs on the endothelial dysfunction associated with altered NO metabolism in cardiovascular diseases.

中文翻译：

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牛磺酸和牛磺酸结合的胆汁酸对内皮源性一氧化氮产生和活性的调节。

牛磺酸是一种在哺乳动物血浆和细胞中高浓度的半必需氨基酸，它调节细胞功能，例如离子通量，控制细胞体积，并用作共轭胆汁酸（BAs）的底物。牛磺酸和牛磺酸结合的BA的外源给药也与心血管功能的调节有关。这篇简短的综述总结了牛磺酸和牛磺酸结合的BAs通过调节内皮源性一氧化氮（NO）在血管舒张中的作用。牛磺酸对血管健康的影响是有争议的。但是，在存在心脏代谢危险因素的情况下，有人提出牛磺酸可以通过增加eNOS的表达，Ser1177上eNOS的磷酸化，NO的生物利用度，抗氧化防御的水平，和1-精氨酸/ NOS抑制剂的不对称二甲基精氨酸（ADMA）比率。牛磺酸结合的BA介导的法呢类X受体（FXR），G蛋白偶联的BA受体（TGR5）和/或毒蕈碱3受体（M3）的激活也增加了血管NO的产生。FXR激活增加eNOS的表达并可能减少ADMA的形成，而TGR5增加内皮细胞中Ca2 +的动员以及eNOS和Akt的磷酸化。此外，牛磺酸和牛磺酸结合的BAs可能通过增强H2S的产生来调节NO的合成和活性。多项研究表明，牛磺酸和牛磺酸结合的BA均可逆转与糖尿病，动脉粥样硬化，高血压，肥胖，营养不良和吸烟有关的内皮功能障碍。此外，牛磺酸结合的BAs已经成为门脉高压症的一种潜在治疗方法。尽管有这些有利的发现，但仍需要进一步探索牛磺酸和牛磺酸结合的BA的内皮作用的机制和信号传导途径。在这里，我们总结了有关牛磺酸和牛磺酸结合的BA对心血管疾病中与NO代谢改变相关的内皮功能障碍的影响的主要发现。