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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Modulation of endothelium-derived nitric oxide production and activity by taurine and taurine-conjugated bile acids

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Guizoni, Daniele M. [1] ; Vettorazzi, Jean F. [2] ; Carneiro, Everardo M. [1, 2] ; Davel, Ana Paula [1]
Total Authors: 4
[1] Univ Estadual Campinas, Inst Biol, Dept Struct & Funct Biol, UNICAMP, Campinas, SP - Brazil
[2] Univ Estadual Campinas, Sao Paulo Res Fdn FAPESP, Obes & Comorbid Res Ctr, Inst Biol, UNICAMP, Dept Struct & Funct Biol, Campinas, SP - Brazil
Total Affiliations: 2
Document type: Journal article
Source: NITRIC OXIDE-BIOLOGY AND CHEMISTRY; v. 94, p. 48-53, JAN 1 2020.
Web of Science Citations: 1

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 (BM). 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. (AU)

FAPESP's process: 13/07607-8 - OCRC - Obesity and Comorbidities Research Center
Grantee:Licio Augusto Velloso
Support type: Research Grants - Research, Innovation and Dissemination Centers - RIDC
FAPESP's process: 14/01717-9 - Investigation of the insulinotropic, insulinomimetic and endothelial actions of taurine in cells/tissues submitted to an in vitro amino acid restriction: an integrated and multifocal approach
Grantee:Everardo Magalhães Carneiro
Support type: Research Projects - Thematic Grants
FAPESP's process: 16/14461-8 - In vivo and in vitro endothelial effects of taurine in protein restriction
Grantee:Daniele Mendes Guizoni
Support type: Scholarships in Brazil - Post-Doctorate